[ Index ]

Note: Search keywords = "Danish Dementia"

(73 References)

Sanchez-Pulido, L., D. Devos, et al. (2002). "BRICHOS: a conserved domain in proteins associated with dementia, respiratory distress and cancer." Trends Biochem Sci 27(7): 329-32.

            A novel domain (the BRICHOS domain) of approximately 100 amino acids has been identified in several previously unrelated proteins that are linked to major diseases. These include BRI(2), which is related to familial British and Danish dementia (FBD and FDD); Chondromodulin-I (ChM-I), related to chondrosarcoma; CA11, related to stomach cancer; and surfactant protein C (SP-C), related to respiratory distress syndrome (RDS). In several of these, the conserved BRICHOS domain is located in the propeptide region that is removed after proteolytic processing. Experimental data suggest that the role of this domain could be related to the complex post-translational processing of these proteins.

Revesz, T., J. L. Holton, et al. (2002). "Sporadic and familial cerebral amyloid angiopathies." Brain Pathol 12(3): 343-57.

            Cerebral amyloid angiopathy (CAA) is the term used to describe deposition of amyloid in the walls of arteries, arterioles and, less often, capillaries and veins of the central nervous system. CAAs are an important cause of cerebral hemorrhage and may also result in ischemic lesions and dementia. A number of amyloid proteins are known to cause CAA. The most common sporadic CAA, caused by A beta deposition, is associated with aging and is a common feature of Alzheimer disease (AD). CAA occurs in several familial conditions, including hereditary cerebral hemorrhage with amyloidosis of Icelandic type caused by deposition of mutant cystatin C, hereditary cerebral hemorrhage with amyloidosis Dutch type and familial AD with deposition of either A beta variants or wild-type A beta, the transthyretin-related meningo-vascular amyloidoses, gelsolin as well as familial prion disease-related CAAs and the recently described BRI2 gene-related CAAs in familial British dementia and familial Danish dementia. This review focuses on the morphological, biochemical, and genetic aspects as well as the clinical significance of CAAs with special emphasis on the BRI2 gene-related cerebrovascular amyloidoses. We also discuss data relevant to the pathomechanism of the different forms of CAA with an emphasis on the most common A beta-related types.

Nilsson, F. M., L. V. Kessing, et al. (2002). "Enduring increased risk of developing depression and mania in patients with dementia." J Neurol Neurosurg Psychiatry 73(1): 40-4.

            OBJECTIVE: To investigate the time relation between dementia and major affective disorders (major depression and mania). METHODS: Register linkage study of the Danish Hospital Register and the Danish Psychiatric Central Research Register, to establish study cohorts of patients with dementia and control groups (osteoarthritis or diabetes) on first discharge from hospital. Follow up of cohorts was for up to 21 years. Hazard of death was allowed for by the use of competing risks models. RESULTS: Patients with dementia had an increased risk of being admitted to hospital for major depression or mania during the course of the illness. The incidence remained elevated throughout the rest of the patient's life. CONCLUSIONS: Patients with dementia have an increased risk of developing depression or mania. Proper treatment of affective disorders in patients with dementia is important in reducing suffering and costs.

Madsen, A. M., R. K. Lomholt, et al. (2002). "[Diagnosis and treatment of Lewy body dementia]." Ugeskr Laeger 164(18): 2383-6.

            Dementia with Lewy bodies (DLB) has recently gained recognition as a separate disease. Lewy bodies are pathoanatomical inclusion bodies in the CNS. They are well known as part of Parkinson's disease where they are present mainly in the substantia nigra, and they are also found in large numbers in the neocortex. It is still an unanswered question why Lewy bodies are formed, but their appearance is connected with cellular degeneration of unknown aetiology. Neuropathological investigations of dementia populations show that DLB accounts for 12-36%, which places it as the second most frequent dementia disease after Alzheimer's disease (AD) with a frequency close to that of vascular dementia. This article reviews the development of the term DLB and describes the clinical characteristics, including the neuropsychological symptom profile, which can contribute to the diagnostic discrimination between DLB and AD. Furthermore, relevant treatment possibilities are discussed.

Kim, S. H., J. W. Creemers, et al. (2002). "Proteolytic processing of familial British dementia-associated BRI variants: evidence for enhanced intracellular accumulation of amyloidogenic peptides." J Biol Chem 277(3): 1872-7.

            Different mutations in the BRI(2) gene cause rare neurodegenerative conditions, termed familial British dementia (FBD) and familial Danish dementia (FDD). The mutant genes encode BRI-L and BRI-D, the precursors of fibrillogenic ABri and ADan peptides, respectively. We previously reported that furin processes both BRI-L and its wild type counterpart, BRI, resulting in the secretion of C-terminal peptides; elevated levels of peptides were generated from BRI-L. In the present study, we show that inducible expression of alpha1-antitrypsin Portland, a furin inhibitor, inhibits the endoproteolysis of BRI and BRI-L in a dose-dependent manner. Moreover, comparison of the activities of several proprotein convertases reveals that furin is most efficient in endoproteolysis of BRI and BRI-L; PACE4, PC6A, PC6B, and LPC show much lower activities. Interestingly, LPC also exhibits enhanced cleavage of BRI-L compared with BRI. Finally, we demonstrate that BRI-D is also processed by furin and, like BRI-L, the cleavage of BRI-D is more efficient than that of BRI. Interestingly, while the ABri peptide is detected both intracellularly and in the medium, the ADan peptide accumulates predominantly in intracellular compartments. We propose that intracellular accumulation of amyloidogenic ADan or ABri peptides results in the neuronal damage leading to FDD and FBD, respectively.

Jorgensen, V. R. and P. Rosted (2002). "[Schiotz's tonometer, a possible source of transmission of prion disease]." Ugeskr Laeger 164(21): 2778.

Jorgensen, V. R. and P. Rosted (2002). "[Prion diseases in general practice--where are the authorities?]." Ugeskr Laeger 164(21): 2779; discussion 2779-80.

Holton, J. L., T. Lashley, et al. (2002). "Familial Danish dementia: a novel form of cerebral amyloidosis associated with deposition of both amyloid-Dan and amyloid-beta." J Neuropathol Exp Neurol 61(3): 254-67.

            Familial Danish dementia (FDD) is pathologically characterized by widespread cerebral amyloid angiopathy (CAA), parenchymal protein deposits, and neurofibrillary degeneration. FDD is associated with a mutation of the BRI2 gene located on chromosome 13. In FDD there is a decamer duplication, which abolishes the normal stop codon, resulting in an extended precursor protein and the release of an amyloidogenic fragment, ADan. The aim of this study was to describe the major neuropathological changes in FDD and to assess the distribution of ADan lesions, neurofibrillary pathology, glial, and microglial response using conventional techniques, immunohistochemistry, confocal microscopy, and immunoelectron microscopy. We showed that ADan is widely distributed in the central nervous system (CNS) in the leptomeninges, blood vessels, and parenchyma. A predominance of parenchymal pre-amyloid (non-fibrillary) lesions was found. Abeta was also present in a proportion of both vascular and parenchymal lesions. There was severe neurofibrillary pathology, and tau immunoblotting revealed a triplet electrophoretic migration pattern comparable with PHF-tau. FDD is a novel form of CNS amyloidosis with extensive neurofibrillary degeneration occurring with parenchymal, predominantly pre-amyloid rather than amyloid, deposition. These findings support the notion that parenchymal amyloid fibril formation is not a prerequisite for the development of neurofibrillary tangles. The significance of concurrent ADan and Abeta deposition in FDD is under further investigation.

Bruunsgaard, H., L. Ostergaard, et al. (2002). "Proinflammatory cytokines, antibodies to Chlamydia pneumoniae and age-associated diseases in Danish centenarians: is there a link?" Scand J Infect Dis 34(7): 493-9.

            Plasma levels of tumour necrosis factor (TNF)-alpha levels increase with age. High levels are associated with dementia and atherosclerosis in centenarians. Chlamydia pneumoniae induces the production of proinflammatory cytokines and has been related to the pathogeneses of Alzheimer's disease and cardiovascular diseases. The purpose of this study was to test the hypothesis that circulating levels of TNF-alpha represent a link between C. pneumoniae, high prevalences of dementia and cardiovascular diseases in 126 Danish centenarians. IgA antibody titres against C. pneumoniae were linearly correlated with high plasma levels of TNF-alpha in centenarians. However, both parameters were also correlated with total IgA in the blood and the association between C. pneumoniae IgA and TNF-alpha was not significant when total IgA was included in a multiple linear regression model. Accordingly, the association between C. pneumoniae-specific IgA and TNF-alpha may reflect immune activation rather than a specific antibody response. No associations were found between antibodies to C. pneumoniae and dementia or cardiovascular diseases. Although TNF-alpha is likely to be involved in the pathogenesis of atherosclerosis and dementia, the present study does not support the hypothesis that TNF-alpha represents a link between chronic C. pneumoniae infection and these disorders.

Trier, H. (2001). "[Renewal of driver's licence: licence suspended for two of five "possibly demented" drivers]." Ugeskr Laeger 163(34): 4604-5.

Tranebjaerg, L., P. K. Jensen, et al. (2001). "Neuronal cell death in the visual cortex is a prominent feature of the X-linked recessive mitochondrial deafness-dystonia syndrome caused by mutations in the TIMM8a gene." Ophthalmic Genet 22(4): 207-23.

            The Mohr-Tranebjaerg syndrome (MIM 304700) and the Jensen syndrome (MIM 311150) were previously reported as separate X-linked recessive deafness syndromes associated with progressive visual deterioration, dystonia, dementia, and psychiatric abnormalities. In the most extensively studied Norwegian family, the Mohr-Tranebjaerg syndrome was reported to be caused by a one-basepair deletion (151delT) in the deafness/dystonia peptide (DDP) gene at Xq22. This gene has been renamed TIMM8a. We identified a stop mutation (E24X) in the TIMM8a gene segregating with the disease in the original Danish family with the Jensen syndrome, which confirms that the two disorders are allelic conditions. We also report abnormal VEP examinations and neuropathological abnormalities in affected males from the two unrelated families with different mutations. The findings included neuronal cell loss in the optic nerve, retina, striate cortex, basal ganglia, and dorsal roots of the spinal cord. The demonstration of mitochondrial abnormalities in skeletal muscle biopsies in some patients is compatible with the suggestion from recent research that the TIMM8a protein is the human counterpart of an intermembrane mitochondrial transport protein, Tim8p, recently characterized in yeast. The clinical and neuropathological abnormalities associated with mutations in the TIMM8a gene support that this X-linked deafness-dystonia-optic neuropathy syndrome is an example of progressive neurodegeneration due to mutations in a nuclear gene necessary for some, yet unknown mitochondrial transport function. We recommend sequencing the TIMM8a gene, thorough ophthalmological examination, and measuring visual evoked potentials in clinically suspected male patients with either progressive hearing impairment, dystonia, or visual disability in order to establish an early diagnosis and provide appropriate genetic counselling.

Sorensen, L., A. Foldspang, et al. (2001). "Determinants for the use of psychotropics among nursing home residents." Int J Geriatr Psychiatry 16(2): 147-54.

            PURPOSE: To characterise the prescription pattern of psychotropics in Danish nursing homes and to identify diagnostic, behavioural, cognitive and performance characteristics associated with prevalent psychotropic drug use. METHODS: Prescribed daily medication was recorded from nurses' files. Based on the Anatomical Therapeutical Chemical (ATC) classification index, psychotropics were categorised into neuroleptics, benzodiazepines and antidepressants. Two hundred and eighty-eight residents were diagnosed using the GMS-AGECAT. One hundred and eighteen staff members were interviewed about the residents's Activities of Daily Living (ADL), behavioural problems (Nursing Home Behavior Problem Scale), orientation, communication skills and if the resident had any psychiatric disorder. Multiple logistic regression was used to select the items that determined the use of psychotropics. RESULTS: Fifty-six percent of the residents received a psychotropic, 21% received neuroleptics, 38% received benzodiazepines and 24% received antidepressants. In the multivariate analysis, staff assessment of the resident's mental health was a determinant for the use of all types of specific psychotropics, whereas a GMS-AGECAT diagnosis only determined the use of neuroleptics. Behavioural problems were a determinant for the use of neuroleptics and the use of benzodiazepines irrespective of the psychiatric diagnosis of the resident. Use of antidepressants was associated with male gender and increasing age. CONCLUSIONS: Staff perceptions of psychiatric morbidity and norms have a greater impact on the prescription of psychotropics than standardised clinical criteria.

Rubak, J. M. (2001). "[Investigation of demented patients. New possibility for improved quality in cooperation between general practice and hospitals]." Ugeskr Laeger 163(3): 274.

Norby, S. (2001). "[Creutzfeldt-Jakob disease]." Ugeskr Laeger 164(1): 75-6.

McGue, M. and K. Christensen (2001). "The heritability of cognitive functioning in very old adults: evidence from Danish twins aged 75 years and older." Psychol Aging 16(2): 272-80.

            Heritable influences on cognitive functioning were investigated in a sample of 403 pairs of like-sex Danish twins aged 75 years and older. Twins completed the Mini-Mental State Examination and 3 other cognitive tests. Genetic factors accounted for 26-54% of the variance on these measures, with the balance being due to environmental factors that create differences rather than similarities among reared-together relatives. Deleting twins with severe cognitive impairment had little effect on the results, indicating that the heritability of cognitive functioning was not due entirely to genes affecting dementia. Neither age nor gender moderated twin similarity, and differential social contact could not account for correlation differences between monozygotic and dizygotic twins. These results replicate G. E. McClearn et al.'s (1997) study in indicating substantial genetic influences on late-life cognitive functioning.

Jorgensen, V. R. and P. Rosted (2001). "[Non-disposable acupuncture needles are potential hazards of transmission of prion diseases]." Ugeskr Laeger 163(9): 1295-6.

Jorgensen, V. R. and P. Rosted (2001). "[Human albumin, a possible way of transmission of prion disease]." Ugeskr Laeger 163(34): 4598; discussion 4598-9.

Johansen, C. (2001). "[Exposure to electromagnetic fields and risk of central nervous system diseases among employees at Danish electric companies]." Ugeskr Laeger 164(1): 50-4.

            INTRODUCTION: Occupational exposure to electromagnetic fields has been associated with neurological diseases, such as amyotrophic lateral sclerosis, senile dementia, Parkinson's disease and Alzheimer's disease. MATERIAL AND METHOD: I studied the incidence of disease in the central nervous system in 30,631 persons employed at Danish electric companies between 1900 and 1993. I linked the cohort to the nationwide, population-based Danish National Register of Patients and compared the number of cases of these diseases found between 1978 and 1993 with the corresponding rates in the general population. In addition, I fit the data on utility workers to a multiplicative Poisson regression model in relation to estimated levels of exposure to 50 Hz electromagnetic fields. RESULTS: Overall, there was an increase in the risk of senile dementia and motor neuron diseases combined. The incidences of Parkinson's disease, Alzheimer's disease and other diseases of the central nervous system were essentially unrelated to exposure to electromagnetic fields. A decreased risk of epilepsy compared with the general population probably reflects a healthy worker effect; I observed an increased risk of epilepsy based on internal comparisons. DISCUSSION: The increased risk of senile dementia and motor neuron diseases may be associated with above average levels of exposure to electromagnetic fields.

Holm, I. E., K. Abelskov, et al. (2001). "Creutzfeldt-Jakob disease segregating in a three generation Danish family." Acta Neurol Scand 103(3): 139-47.

            A three generation family is presented in which rapidly progressive, early-onset Creutzfeldt-Jakob disease without typical EEG changes segregates as an autosomal dominant disease. An aspartic acid to asparagine mutation at codon 178 of the prion gene, PRNP, co-segregates with the disease. As expected, the disease allele also carries the valine codon of the polymorphic valine/methionine codon 129 of the gene. In family members homozygous for this valine codon the disease was more rapidly progressive than in a heterozygous family member, who had a variant clinical phenotype. Definite neuropathological diagnosis required prion staining with specific antibodies.

Hansen, N. J. (2001). "[Mister Creutzfeldt--he is known! But where is Mister Jacob?]." Ugeskr Laeger 164(1): 75.

Grandjean, P. (2001). "[Blood donors and vCJD]." Ugeskr Laeger 163(39): 5389-90.

Ghiso, J., T. Revesz, et al. (2001). "Chromosome 13 dementia syndromes as models of neurodegeneration." Amyloid 8(4): 277-84.

            Two hereditary conditions, familial British dementia (FBD) and familial Danish dementia (FDD), are associated with amyloid deposition in the central nervous system and neurodegeneration. The two amyloid proteins, ABri and ADan, are degradation products of the same precursor molecule BriPP bearing different genetic defects, namely a Stop-to-Arg mutation in FBD and a ten-nucleotide duplication-insertion immediately before the stop codon in FDD. Both de novo created amyloid peptides have the same length (34 amino acids) and the same post-translational modification (pyroglutamate) at their N-terminus. Neurofibrillary tangles containing the classical paired helical filaments as well as neuritic components in many instances co-localize with the amyloid deposits. In both disorders, the pattern of hyperphosphorylated tau immunoreactivity is almost indistinguishable from that seen in Alzheimer's disease. These issues argue for the primary importance of the amyloid deposits in the mechanism(s) of neuronal cell loss. We propose FBD and FDD, the chromosome 13 dementia syndromes, as models to study the molecular basis of neurofibrillary degeneration, cell death and amyloid formation in the brain.

Ghiso, J. and B. Frangione (2001). "Cerebral amyloidosis, amyloid angiopathy, and their relationship to stroke and dementia." J Alzheimers Dis 3(1): 65-73.

            Cerebral amyloid angiopathy (CAA) is the common term used to define the deposition of amyloid in the walls of medium- and small-size leptomeningeal and cortical arteries, arterioles and, less frequently, capillaries and veins. CAA is an important cause of cerebral hemorrhages although it may also lead to ischemic infarction and dementia. It is a feature commonly associated with normal aging, Alzheimer disease (AD), Down syndrome (DS), and Sporadic Cerebral Amyloid Angiopathy. Familial conditions in which amyloid is chiefly deposited as CAA include hereditary cerebral hemorrhage with amyloidosis of Icelandic type (HCHWA-I), familial CAA related to Abeta variants, including hereditary cerebral hemorrhage with amyloidosis of Dutch origin (HCHWA-D), the transthyretin-related meningocerebrovascular amyloidosis of Hungarian and Ohio kindreds, the gelsolin-related spinal and cerebral amyloid angiopathy, familial PrP-CAA, and the recently described chromosome 13 familial dementia in British and Danish kindreds. This review focuses on the various molecules and genetic variants that target the cerebral vessel walls producing clinical features related to stroke and/or dementia, and discusses the potential role of amyloid in the mechanism of neurodegeneration.

Gerstoft, J. and E. Dickmeiss (2001). "[The significance of bovine spongiform encephalopathy epidemics for transfusion medicine]." Ugeskr Laeger 163(22): 3048.

Frangione, B., T. Revesz, et al. (2001). "Familial cerebral amyloid angiopathy related to stroke and dementia." Amyloid 8 Suppl 1: 36-42.

            The term cerebral amyloid angiopathy (CAA) refers to the specific deposition of amyloid fibrils in the walls of leptomeningeal and cortical arteries, arterioles and, although less frequently in capillaries and veins. It is commonly associated with Alzheimers disease, Down's syndrome and normal aging, as well as with a variety of familial conditions related to stroke and/or dementia: hereditary cerebral hemorrhage with amyloidosis of Icelandic type (HCHWA-I), various inherited disorders linked to Abeta mutants (including the Dutch variant of HCHWA), and the recently described chromosome 13 familial dementia in British and Danish kindreds. This review focuses on four different types of hereditary CAA, emphasizing the notion that CAA is not only related to stroke but also to neurodegeneration and dementia of the Alzheimer's type.

Christoffersen, B. R. and J. Jansen (2001). "[Creutzfeldt-Jakob syndrome in the county of Storstrom during the period 1990-1999. Was there a significant accumulation of cases?]." Ugeskr Laeger 163(45): 6275-9.

            INTRODUCTION: In the county of Storstrom with about 250,000 inhabitants, ten cases of Creutzfeldt-Jacob disease (CJD) were diagnosed at the Department of Neurology, Naestved County Hospital during the decade 1990-1999. Only one case is to be expected every four years in the county. Therefore we decided to investigate if a significant accumulation had occurred. METHODS: Case records were examined to see whether the patients complied with the WHO criteria for possible, probable, or certain sporadic CJD. Poisson distribution with correction for age was used to compare the observed incidence with the expected incidence of 1 case/million/year. RESULTS: Eight cases complied with the diagnostic criteria: two certain, three probable, two possible, and one familial. The incidence of certain and probable cases was 1.9 per million per year during the period, which does not constitute a significant increase (p = 0.18). CONCLUSION: The result is consistent with the fact that all time or space clustering of CJD ever reported has proved ascribable to familial cases, and with the fact that case-control studies have never identified environmental risk factors for sporadic CJD.

Andersen-Ranberg, K., L. Vasegaard, et al. (2001). "Dementia is not inevitable: a population-based study of Danish centenarians." J Gerontol B Psychol Sci Soc Sci 56(3): P152-9.

            The authors evaluated the prevalence of dementia in centenarians. In this population-based survey, persons living in Denmark who turned 100 during the period April 1, 1995--May 31, 1996 (N = 276) were interviewed and examined at their residences. Additional health information was retrieved from medical files, including the National Discharge Registry. A participation rate was 75%, and no differences were found between participants and nonparticipants regarding sex and type of housing. The prevalence of mild to severe dementia in centenarians was 51%; 37% had no signs of dementia. Among the 105 demented centenarians, 13 (12%) had diseases (vitamin B12 and folic acid deficiencies, hypothyroidism, Parkinson's disease) that could contribute to a dementia diagnosis. Of the remaining 92 demented participants, 46 (50%) had 1 one or more cerebro- or cardiovascular diseases known to be risk factors in the development of dementia. The prevalence of these risk factors was the same in demented and nondemented participants, whereas hypertension was significantly more frequent in nondemented than demented participants. Dementia is common but not inevitable in centenarians. Cerebro- and cardiovascular diseases are equally common in demented and nondemented persons.

Andersen-Ranberg, K., M. Schroll, et al. (2001). "Healthy centenarians do not exist, but autonomous centenarians do: a population-based study of morbidity among Danish centenarians." J Am Geriatr Soc 49(7): 900-8.

            OBJECTIVE: To assess the prevalence of common illnesses in an unselected population of centenarians. DESIGN: A population-based survey. SETTING: Denmark. PARTICIPANTS: All Danes who celebrated their 100th anniversary between April 1, 1995 and May 31, 1996: 276 persons. MEASUREMENTS: All participants (including proxies) were visited at their domicile for an interview (sociodemographic characteristics, activities of daily living, living conditions, need of assistance from other people, former health and current diseases, current medication) and a clinical examination (dementia screening test, heart and lung auscultation, neurological assessment, height and weight, electrocardiogram, arm and ankle blood pressure, assessment of hearing and vision capacity, a short physical performance test, bio-impedance, lung function test, blood test). Further health information was retrieved from medical files and national health registers. RESULTS: Seventy-five percent (207) of eligible subjects participated in the study. Cardiovascular disease was present in 149 (72%) subjects. Osteoarthritis (major joints) was present in 54%, hypertension (> or =140/ > or =90) in 52%, dementia in 51%, and ischemic heart disease in 28%. The mean number of illness was 4.3 (standard deviation (SD) 1.86). Only one subject was identified as being free from any chronic condition or illness. Sixty percent had been treated for illness with high mortality. In 25 autonomous (nondemented, functioning well physically, living at home) and 182 nonautonomous centenarians, comorbidities were equivalent. CONCLUSION: Because they have a high prevalence of several common diseases and chronic conditions, Danish centenarians are not healthy. However, a minor proportion was identified as being cognitively intact and functioning well.

Viftrup, J. E. and B. O. Pedersen (2000). "[Dementia and pseudodementia in the municipality of Ringkobing]." Ugeskr Laeger 162(23): 3334-8.

            Social services estimated on September 1, 1997 that 221 individuals out of a population of about 16,000 in the whole of Ringkobing County were believed to suffer from dementia. Citizens believed to suffer from dementia were offered an assessment by a trained nurse and a general practitioner. In the following six months, 119 people were screened by the nurse with the Mini Mental State Examination, the Geriatric Depression Scale-15 and Gottfries-Brane-Steen scale for evaluating functional deficiencies in demented patients. In addition, somatic and laboratory screening was done by the GP's. Approximately 40 citizens or 33% were not found to suffer from dementia but suffered from other illnesses. One year later all the GP's answered questionnaires concerning number of cases of depression, hypothyroidism, vitamin B12 deficiency or other illnesses not earlier known to the GP. Twenty-two diseases were identified and six patients improved.

Vidal, R., T. Revesz, et al. (2000). "A decamer duplication in the 3' region of the BRI gene originates an amyloid peptide that is associated with dementia in a Danish kindred." Proc Natl Acad Sci U S A 97(9): 4920-5.

            Familial Danish dementia (FDD), also known as heredopathia ophthalmo-oto-encephalica, is an autosomal dominant disorder characterized by cataracts, deafness, progressive ataxia, and dementia. Neuropathological findings include severe widespread cerebral amyloid angiopathy, hippocampal plaques, and neurofibrillary tangles, similar to Alzheimer's disease. N-terminal sequence analysis of isolated leptomeningeal amyloid fibrils revealed homology to ABri, the peptide originated by a point mutation at the stop codon of gene BRI in familial British dementia. Molecular genetic analysis of the BRI gene in the Danish kindred showed a different defect, namely the presence of a 10-nt duplication (795-796insTTTAATTTGT) between codons 265 and 266, one codon before the normal stop codon 267. The decamer duplication mutation produces a frame-shift in the BRI sequence generating a larger-than-normal precursor protein, of which the amyloid subunit (designated ADan) comprises the last 34 C-terminal amino acids. This de novo-created amyloidogenic peptide, associated with a genetic defect in the Danish kindred, stresses the importance of amyloid formation as a causative factor in neurodegeneration and dementia.

Sorensen, L., A. Foldspang, et al. (2000). "[Nursing home residents in Northern Jutland]." Ugeskr Laeger 162(10): 1393-8.

            The purpose of the study was to describe a Danish nursing home population. The study consists of 288 nursing home residents (median age 84.6 years, 68% females). The psychiatric morbidity of the residents was diagnosed with the GMS-AGECAT. The staff was interviewed about the residents' ADL, disturbing behaviour and therapeutic measures. Seventy-one percent had a psychiatric disorder, with organic disorder as the most frequent (61%). Demented residents received significantly less hypnotics, were more often physically restrained and had lower ADL levels compared to other residents. The situation in Denmark can be seen as a paradox. While substantial effort has been made to increase the possibility of choice and to "deinstitutionalize" nursing homes, the majority of the residents are demented and thus not capable of making valid choices.

Norrung, B. and P. Willeberg (2000). "[Mad cow disease/bovine spongiform encephalopathy]." Ugeskr Laeger 162(34): 4518-9.

Linde, J. (2000). "[Prevalence of dementia in Denmark]." Ugeskr Laeger 162(45): 6106-7.

Johansen, C. (2000). "Exposure to electromagnetic fields and risk of central nervous system disease in utility workers." Epidemiology 11(5): 539-43.

            Occupational exposure to electromagnetic fields has been associated with neurological diseases such as amyotrophic lateral sclerosis, senile dementia, Parkinson disease, and Alzheimer disease. I studied the incidence of central nervous system diseases in 30,631 persons employed in Danish utility companies between 1900 and 1993. I linked the cohort to the nationwide, population-based Danish National Register of Patients and compared the numbers of cases of these diseases observed between 1978 and 1993 with the corresponding rates in the general population. In addition I fit to the data on utility workers a multiplicative Poisson regression model in relation to estimated levels of exposure to 50-Hz electromagnetic fields. Overall, there was an increase in risk for senile dementia and motor neuron diseases combined. The incidences of Parkinson disease, Alzheimer disease, and other diseases of the central nervous system were essentially unrelated to exposure to electromagnetic fields. A decreased risk of epilepsy compared with the general population probably reflects a healthy worker effect; I observed an increased risk of epilepsy based on internal comparisons. The increased risk for senile dementia and motorneuron diseases may be associated with above-average levels of exposure to electromagnetic fields.

Gerstoft, J. (2000). "[Transmission of bovine spongiform encephalopathy prions to human]." Ugeskr Laeger 162(34): 4515-7.

Garde, E., E. L. Mortensen, et al. (2000). "Relation between age-related decline in intelligence and cerebral white-matter hyperintensities in healthy octogenarians: a longitudinal study." Lancet 356(9230): 628-34.

            BACKGROUND: White-matter hyperintensities are commonly found on magnetic resonance imaging (MRI) of elderly people with or without dementia. Studies of the relation between severity of white-matter hyperintensities and cognitive impairment have had conflicting results. We undertook a longitudinal study of age-related decline in intellectual function and MRI at age 80 years. METHODS: From a cohort of 698 people born in 1914 and living in seven municipalities in Denmark, 68 healthy non-demented individuals had been tested with the Wechsler adult intelligence scale (WAIS) at ages 50, 60, and 70, and they agreed to further WAIS testing at age 80, and cerebral MRI at age 80-82 (mean age 82.3 years). We scored separately the numbers of periventricular and deep white-matter hyperintensities. FINDINGS: Scores for periventricular hyperintensities in this sample included all possible degrees of severity, but no participant scored more than 75% of maximum for deep white-matter hyperintensities. Neither type was related to the WAIS IQs of the 80-year assessment, but both were significantly associated with decline in performance IQ from age 50 to age 80 years (bivariate correlation coefficients 0.32, p=0.0087, and 0.28, p=0.0227, respectively). An analysis based on two WAIS subtests showed that the association between white-matter hyperintensities and cognitive impairment was significant only for cognitive decline in the decade 70-80 years. INTERPRETATION: Both periventricular and deep white-matter hyperintensities are related to decline in intelligence but, in healthy octogenarians, the cumulative effect of these features alone explains only a small part of the large differences among individuals in age-related decline in intelligence. Interpretation of the presence and severity of white-matter hyperintensities in a diagnostic context must be done cautiously.

Binzer, M. N., L. Brattstrom, et al. (2000). "[Clinical, radiological, histopathological and genetic findings in a Danish "CADASIL" family]." Ugeskr Laeger 162(12): 1739-42.

            Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a rare adult-onset inherited arterial disease with a distinctive neuropathological phenotype. Owing to its recent identification and variable mode of presentation, the disease is often misdiagnosed. The CADASIL gene is Notch 3 and has been mapped on chromosome 19q12 in several unrelated families. Knowledge of the phenotypic range of CADASIL, however, remains incomplete. Clinical, pathological radiological, and genetic findings in the first known Danish CADASIL pedigree are presented. Genetic testing confirmed a Notch 3 mutation. The mutation consisted of the substitution of a nucleotide at position 475 leading to the replacement of amino acid arginine for cysteine at position 133 in the third EGF motif.

Andersen, K., A. Lolk, et al. (2000). "[Prevalence and incidence of dementia in Denmark. The Odense study]." Ugeskr Laeger 162(33): 4386-90.

            Prevalence and incidence of dementia were determined for 65-84 year-old persons living in the municipality of Odense and randomly drawn from the Danish Civil Registration System (DCRS). All participants were examined with CAMCOG, the cognitive section of CAMDEX (The Cambridge Examination for Mental Disorders of the Elderly) and the follow-up period was two years. Individualized CAMCOG cut-off scores were determined by multiple linear regression. Possibly demented persons were further examined with the remaining part of CAMDEX and neuropsychological tests. Alzheimer's disease (AD) was diagnosed according to the NINCDS-ADRDA criteria for probable AD, and vascular dementia (VD) and dementias of other types according to the DSM-III-R criteria for dementia. The severity of dementia was determined according to the Clinical Dementia Rating scale. Of the 5,237 persons drawn from the DCRS, 3,346 participated in the prevalence study and 2,452 in the incidence study. The prevalence was 7.1% (66.7% AD, 18.3% VD, and 15.0% dementias of other types). Ninety-six (2.8%) were diagnosed as very mildly demented. The incidence rate was 29.5 new cases per 1,000 person-years and 20.9 for AD. Inclusion of cases with very mild dementia resulted in higher prevalence and incidence rates than generally reported.

Waldorff, F. B. and O. Dinesen (1999). "[Referral from general practice to diagnostic evaluation of dementia]." Ugeskr Laeger 161(38): 5304-7.

            The study objective was to describe the GP's referrals of patients to diagnostic evaluation of dementia and the GP's perception of the organization of this process++. The study is based on postal questionnaire mailed to all GPs in Denmark, spring 1998. Seventy-five percent of 3379 GPs answered the questionnaire. Seventy-one percent (1799) of the GPs had referred a patient to diagnostic evaluation of dementia within the last 12 months. Thirty-nine percent had referred to a geriatric psychiatric service, 36% to a neurologic service, 18% to a psychiatric service, 11% to a geriatric service, and 16% had referred to other services. Fifteen percent of the GPs had referred to two or more of the services. The study concludes that there is considerable regional variation as to where the GPs refer patients for diagnostic evaluation of dementia as well as to the GPs perception of the possibilities of referrals in Denmark. The implications are discussed.

Thomsen, J. S., T. Horn, et al. (1999). "[Amyloidosis. A review]." Ugeskr Laeger 161(21): 3079-83.

            Amyloidosis is a heterogenous group of diseases, all characterized by extracellular deposition of amyloid either systemically or localized. Of wellknown diseases are Alzheimer's dementia, AL-amyloidosis (e.g. in multiple myeloma) and AA-amyloidosis (e.g. in rheumatoid arthritis). Amyloid is composed of three components of which the fibrillary component is the basis of amyloid classification. Many types of amyloid have a systemic distribution and give rise to varying symptoms. The diagnosis is based on biopsy, preferably of abdominal subcutis. The prognosis is poor, however, recent investigations on the three-dimensional structure of the P-component provide hope for future therapy.

Romero, I., P. Jorgensen, et al. (1999). "A presenilin-1 Thr116Asn substitution in a family with early-onset Alzheimer's disease." Neuroreport 10(11): 2255-60.

            Mutation in the presenilin-1 (PS-1) gene at chromosome 14q24.3 is the most common cause of autosomal dominant early-onset Alzheimer's disease. Here, we report a novel missense mutation in the presenilin-1 gene found in a three-generation Danish family with autopsy-verified early-onset Alzheimer's disease. Two affected first-degree relatives in two generations were found to be heterozygous for a cytosine to adenine transversion at the second position of codon 116, which changes the amino acid at that position from threonine to asparagine. This conservative amino acid substitution occurs in an evolutionary highly conserved region of the PS-1 protein and is associated with onset of the disease between age 35 and 41 years and 4-8 years' duration of the disease. Analysis of amyloid beta-protein (A beta) deposition in brain specimens from one affected family member showed predominance of A beta 42(43). Onset and progression of the disease were very similar in two sibs homozygous for the epsilon 3 allele and the epsilon 4 allele, respectively, of the polymorphic apolipoprotein E locus. The lack of effect of the high risk epsilon 4/epsilon 4 genotype on the disease in this family corroborates and extends previous observations that the presence of one copy of the epsilon 4 allele does not modulate PS-1 associated Alzheimer's disease.

Philipsen, M., J. V. Rosenbeck-Hansen, et al. (1999). "[Behavioral disorders in nursing home residents. 147 consecutive referrals to an interdisciplinary team of consulting specialists]." Ugeskr Laeger 161(43): 5915-9.

            During a period of 22 months 147 consecutive residents with behavioural disturbances from 80% of the Copenhagen nursing homes were referred to a visiting team of consulting specialists. Each resident was evaluated clinically, and data were recorded in a database. The conditions thought to represent the underlying etiologies were dementia (79%), delirium (28%) and depression (35%). The most commonly observed behavioural symptoms were aggressiveness, vocally disruptive behavior and non-aggressive psychomotor symptoms. The most common interventions suggested by the team were further diagnostic evaluations, adjustment of pharmaceutical treatment, using the life history of the resident as a reference for behaviour management, and psychological behavior management. There is a need for increased focus on systematic diagnosis and treatment of behavioural disorders, observed in nursing homes, which often have multifactorial etiology.

Martiny, K. P. and C. S. Petersen (1999). "[Dementia paralytica is still seen in Denmark]." Ugeskr Laeger 161(18): 2682-3.

            Two cases of neurosyphilis are presented. Both patients had developed a paranoid psychosis and needed admission to a psychiatric department. In both cases relevant treatment resulted in improvement of both the dementia and the psychotic condition, though the patients were left with some degree of dementia at follow up. Both patients had a symptom-free interval lasting several years. It still remains important to take WR, when investigating the cause of dementia, and when dealing with patients admitted to neurological and psychiatric departments with an uncertain diagnosis.

Malling, B. J. (1999). "[Malignant neuroleptic syndrome in patients with dementia]." Ugeskr Laeger 161(17): 2541-2.

            The neuroleptic malignant syndrome (NMS) is a side-effect of treatment with neuroleptic drugs. It is infrequent, but underdiagnosed. The diagnosis can be especially difficult to verify, in older patients with dementia because they often have symptoms of NMS, as a consequence of age and dementia. The importance of monitoring serum-creatine-kinase is discussed and proposals for treatment are suggested.

Lien, K., C. Fensbo, et al. (1999). "[Dementia and psychiatric service]." Ugeskr Laeger 161(38): 5313-6.

            The study objective was to describe the service provision in geriatric psychiatry in 1997 and the trends in admission patterns for the elderly to psychiatric hospitals in Denmark from 1988 to 1996. Information concerning admission pattern was obtained from the Danish Psychiatric Case Register. The information on the supply of geriatric psychiatric services was collected by a questionnaire to the individual geriatric psychiatric departments. All geriatric psychiatric departments in Denmark have been identified. The number of demented patients admitted to psychiatric hospitals decreased considerably as did the length of stay for demented patients admitted from 1988 to 1996. For all other diagnoses the number of admissions increased in the same period. Four counties out of 14 did not have a special unit for geriatric psychiatry. There were considerable geographical variations in supply as well as target groups in the counties that supplied geriatric psychiatric service. The unequal access to geriatric psychiatric services and variations in target groups underlines the need for a discussion of future directions for this service provision.

Kessing, L. V., E. W. Olsen, et al. (1999). "Dementia in affective disorder: a case-register study." Acta Psychiatr Scand 100(3): 176-85.

            OBJECTIVE: The aim of the study was to investigate whether patients with affective disorder have increased risk of developing dementia compared to other groups of psychiatric patients and compared to the general population. METHOD: In the Danish psychiatric central register, 3363 patients with unipolar affective disorder, 518 patients with bipolar affective disorder, 1025 schizophrenic and 8946 neurotic patients were identified according to the diagnosis at the first ever discharge from psychiatric hospital during the period from 1970 to 1974. The rate of discharge diagnosis of dementia on readmission was estimated during 21 years of follow-up. In addition, the rates were compared with the rates for admission to psychiatric hospitals with a discharge diagnosis of dementia for the total Danish population. RESULTS: Patients with unipolar and with bipolar affective disorder had a greater risk of receiving a diagnosis of dementia than patients with schizophrenia and those with neurosis. All groups of patients had a higher risk of being given a diagnosis of dementia than gender- and age-matched samples of the general population. CONCLUSION: Patients with affective disorder appear to be at increased risk of developing dementia.

Fensbo, C., K. Lien, et al. (1999). "[The elderly in general psychiatry]." Ugeskr Laeger 161(19): 2807-10.

            The Danish National Board of Health recommends that the counties offer psychogeriatric services. The target group for geriatric psychiatry in the County of North Jutland only concerns elderly people with severe dementia. It has been our aim to describe and discuss the geriatric psychiatric supply of services and admission pattern for elderly with psychiatric morbidity in the County of North Jutland. We have made a cross-sectional study of all patients referred to the general and psychogeriatric service in 1997. In psychogeriatric service 40 of 46 referrals were dealt with as out-patient contact. In general psychiatry the 57 referrals resulted in 33 admissions of which 31 were acute. There is a high number of acute admissions in general psychiatry. The County of North Jutland does not have a suitable service for diagnostic work-up and treatment of people with possible to moderate dementia.

Djernes, J. K. and N. C. Gulmann (1999). "[Treatment of delirium in a psychogeriatric university hospital department. Etiology, treatment concept and outcome]." Ugeskr Laeger 161(14): 2090-4.

            The purposes of the study were to account for aetiology, treatment concept, outcome of treatment, and discharge destination of delirious elderly inpatients. During one year all patients in a psychogeriatric university department were assessed on admission and at discharge with a selection of assessments measuring psychopathology, behavioural disorders, depressive symptoms, intellectual functioning, activities of daily living, and gait. Diagnoses were made according to the ICD-10 criteria for research. All patients with a principal diagnosis of delirium (n = 26) are accounted for. Delirious patients improved their health status significantly in all the assessments, and 86% of patients admitted from independent living were discharged to independent living. It is concluded that elderly inpatients with severe or prolonged delirium profit significantly from the treatment concept in all of the rated health aspects.

Sorensen, L., A. Foldspang, et al. (1998). "Concurrent validity of the GMS-AGECAT (A3) package in a Danish nursing home population." Int J Geriatr Psychiatry 13(5): 336-42.

            AIM: To validate the Danish version of the GMS-AGECAT (A3), the Standardized Mini Mental State Examination (SMMSE) and the Geriatric Depression Scale-15 (GDS-15) by comparing them to clinical ICD-10 criteria in a Danish nursing home population. METHODS: With a participation of 91%, the study included 100 residents. All residents were interviewed with the GMS-AGECAT (A3), SMMSE and GDS-15 by an MD and then blindly diagnosed by a consultant geriatric psychiatrist. All residents approached for an interview were included, also those who were not able to communicate (the non-accessibles). RESULTS: The prevalence of clinical psychiatric ICD-10 main diagnoses was 56%. The non-accessibles had significantly higher psychiatric morbidity and lower ADL scores (modified Barthel ADL index) compared to those who were able to communicate. With the non-accessibles (N = 100) included, the optimal screening and diagnostic cutpoint for the GMS-AGECAT organic diagnoses was 2/3, with 96% sensitivity, 73% specificity, 77% predictive value of a positive test and 95% predictive value of a negative test. The SMMSE and GDS-15 had better screening properties compared to the GMS-AGECAT but only 60% of the residents were able to complete the SMMSE and 78% were able to complete the GDS-15. CONCLUSION: The Danish version of the GMS-AGECAT has relevant diagnostic and screening properties for organic disorders in Danish nursing home populations.

Sondergaard, H., H. S. Jorgensen, et al. (1998). "["CADASIL"--a newly discovered hereditary cerebrovascular disease]." Ugeskr Laeger 160(11): 1617-20.

            CADASIL (Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leucoencephalopathy) is a newly discovered inherited cerebrovascular disease characterized clinically by recurrent stroke-like incidents, dementia and often pseudobulbar palsy. Neuroimaging reveals intensive subcortical changes and pathologically one finds apparently systemic changes concerning the vessels such as thickening of the vessel wall, loss of smooth muscle cells and patches of granular material of unknown origin. The disease is not associated with atherosclerosis and vascular risk factors are missing or few. The CADASIL-locus maps to chromosome 19, but the gene has not yet been identified. Treatment and pathogenesis are unknown. In a Danish stroke population (The Copenhagen Stroke Study) no CADASIL-suspected cases were found among patients < or = 55 years, indicating a rare disease as far as Denmark is concerned.

Skausig, O. B. and T. Jensen (1998). "[Treatment of dementia]." Ugeskr Laeger 160(11): 1659-60.

Nielsen, A. S., G. Waldemar, et al. (1998). "[Alzheimer's diseases--etiology and pathogenesis]." Ugeskr Laeger 160(22): 3193-7.

Lomholt, R. K. and K. S. Jurgensen (1998). "[The mini-mental state examination in screening of cognitive dysfunction and dementia]." Ugeskr Laeger 160(50): 7251-4.

            The mini-mental state examination (MMSE) is one of the most widely used screening instruments for the detection of cognitive impairments, used primarily in connection with screening for dementia. The intent of this review is to describe the original purpose of the MMSE and how it is currently used in clinical practice and in research. Advantages and limitations of the MMSE in providing a valid diagnosis of cognitive impairments (dementia) are discussed including sensitivity and specificity, the issues of the relationship of the MMSE scores to sociodemographic variables and examinations of factor structures of the MMSE. It is concluded that the MMSE provides a valid diagnosis of cognitive impairments among people with moderate and severe dementia in general populations. However, MMSE is not recommended as a screening instrument for the detection of early stages of dementia. Studies are needed to extend the present knowledge about how or whether the MMSE can be used in the clinical diagnostic evaluation of dementia and how demented patients treated with medications should be monitored.

Lokkegaard, T., J. E. Nielsen, et al. (1998). "Machado-Joseph disease in three Scandinavian families." J Neurol Sci 156(2): 152-7.

            Machado-Joseph disease (MJD) is an autosomal dominantly inherited neurodegenerative disorder characterized by varying age of onset and pronounced phenotypic heterogeneity. The clinical core features include gait ataxia, external ophthalmoplegia, nystagmus, and bulging eyes. Recently, Kawagushi et al. (1994) cloned the MJD1 gene on chromosome 14 and MJD turned out to be the fifth neurodegenerative disease caused by an unstable CAG repeat expansion. We have studied two large Danish families and one Norwegian family with MJD. Three features not previously associated with MJD are reported: dementia, generalized muscle and joint pain, and in one case neuropathological examination revealed atrophy of the inferior olives. We found a significant inverse correlation between age of onset and the length of the CAG repeat expansion, and anticipation is described through four succeeding generations. Instability of the CAG repeat expansion was most pronounced at paternal transmission.

Leth, K. (1998). "[Regulations ensure safety. Interview by Kirsten Bjornsson.]." Sygeplejersken 98(10): 14-5.

Jurgensen, K. S. and R. K. Lomholt (1998). "[Diagnosis of dementia in family practice]." Ugeskr Laeger 160(5): 661-2.

Hjorth-Hansen, J. (1998). "[Provide demented patients with a companion in the system. Interview by Kirsten Bjornsson.]." Sygeplejersken 98(10): 16-7.

Gotfredsen, K. (1998). "[Difficult with ban against code lockup. Interview by Kirsten Bjornsson.]." Sygeplejersken 98(10): 18-9.

Gjedde, A. (1998). "[Bipariental failure in Alzheimer's disease]." Ugeskr Laeger 160(22): 3236-7.

Brown, J. (1998). "Chromosome 3-linked frontotemporal dementia." Cell Mol Life Sci 54(9): 925-7.

            Frontotemporal dementia accounts for a significant minority of all cases of presenile dementia. Many pedigrees have been described in which frontotemporal dementia is inherited as an autosomal dominant trait. Frontotemporal dementia is genetically heterogeneous with loci identified on chromosome 17 and chromosome 3. Clinical, pathological and genetic findings are described in a large Danish family in which the disease gene lies in the pericentromeric region of chromosome 3.

Blicher, J. and H. Pedersen (1998). "[A protest and two proposals]." Ugeskr Laeger 160(39): 5679-80.

Blattler, T., H. Laursen, et al. (1998). "[Does mad cow disease cause the new variant of Creutzfeldt-Jakob disease?]." Nord Med 113(3): 87-93.

Bjornsson, K. (1998). "[Regulations on the way about force against demented patients]." Sygeplejersken 98(10): 10-3.

Bjornsson, K. (1998). "[Overlook hidden medication]." Sygeplejersken 98(10): 20-1, 46.

von Magnus, M. (1997). "[Risk of Creutzfeldt-Jakob syndrome in connection with pulmonary scintigraphy. Patient information]." Ugeskr Laeger 160(1): 60-1.

Sovndal, V. (1997). "[Dementia--the weakest must be protected. Interview by Kirsten Bjornsson.]." Sygeplejersken 97(15): 8-12.

Schulz-Larsen, K. (1997). "[Dementia--urgency in diagnosing it. Interview by Kirsten Bjornsson.]." Sygeplejersken 97(14): 22-7.

Pedersen, U. (1997). "[Violence is violence]." Sygeplejersken 97(45): 20.

Dybdal, K. (1997). "[Quality assurance--standards, self assessment and observation in nursing care of persons with dementia]." Sygeplejersken 97(17): 18-25.

Dahl, O. (1997). "[Good experience with memory course]." Sygeplejersken 97(21): 23.

Blattler, T., H. Laursen, et al. (1997). "[Is crazy cow disease the cause of the new variant of Creutzfeldt-Jakob syndrome?]." Ugeskr Laeger 159(51): 7650-8.

            In 1986, veterinary pathologists discovered spongiform encephalopathy in the brains of two cows in the UK. These two cases turned out to be the beginning of epidemic bovine spongiform encephalopathy (BSE), which culminated in 1992 with more than 3000 cases monthly. In 1996, the British government announced that a distinct variant of CJD (vCJD) had occurred in ten young people in the UK. The cases were notified within the past 1 1/2 years. A link to BSE seemed likely. Transmission studies of the two diseases have demonstrated similar properties such as incubation time, neuropathology and glycoform profile of the pathologically altered prionprotein. In effect, vCJD is very likely to represent human BSE. Epidemiological data suggest that BSE transmission to humans may have occurred only in a limited number of cases. Future studies will have to confirm this. So far, no increase in the incidence of vCJD has been noticed.

Bjornsson, K. (1997). "[More housing for demented patients]." Sygeplejersken 97(49): 16-7.

Riis, P. (1993). "The Danish Brain Collection and its important potentials for future research." Irb 15(6): 5-6.