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208 PRINCIPLES AND PRACTICE OF GERIATRIC PSYCHIATRY47. Launer LJ, Hoes AW. NSAIDs and the risk for Alzheimer’s disease:weighing the epidemiologic evidence. Neurogeriatrics andNeurogerontology, 1998; 133–42.48. Breitner JC, Gau BA, Welsh KA et al. Inverse association of antiinflammatorytreatments and Alzheimer’s disease: initial results of aco-twin control study. Neurology 1994; 44: 227–32.49. Henderson AS, Jorm AF, Christensen H et al. Aspirin, antiinflammatorydrugs and risk of dementia. Int J Geriatr Psychiatry1997; 12: 926–30.50. Fourrier A, Letenneur L, Begaud B, Dartigues JF. Non-steroidalantiinflammatory drug use and cognitive function in the elderly:inconclusive results from a population-based cohort study. J ClinEpidemiol 1996; 49: 1201.51. in’t Veld BA, Launer LJ, Hoes AW et al. NSAIDs and incidentAlzheimer’s disease. The Rotterdam Study. Neurobiol Aging 1998; 19:607–11.52. Stewart WF, Kawas C, Corrada M, Metter EJ. Risk of Alzheimer’sdisease and duration of NSAID use. Neurology 1997; 48: 626–32.53. Goate A, Chartier-Harlin MC, Mullan M et al. Segregation of amissense mutation in the amyloid precursor protein gene with familialAlzheimer’s disease. Nature 1991; 349: 704–6.54. Sherrington R. Cloning of a novel gene bearing missense mutations inearly onset familial Alzheimer’s disease. Nature 1995; 375: 754–60.55. Rogaev E. Familial Alzheimer’s disease in kindreds with missensemutations in a gene on chromosome 1 related to the Alzheimer’sdisease type 3 gene. Nature 1995; 376: 775–8.56. Strittmatter WJ. Apolipoprotein E: high avidity binding to -amyloidand increased frequency of type 4 allele in late-onset familialAlzheimer’s disease. PNAS 1993; 1977–81.57. Alzheimer Research Forum/Research findings/Molecular Genetics ofAlzheimer’s Disease, October, 1999 (http://www.alzforum.org).58. Blacker D, Wilcox MA, Laird NM et al. Alpha-2 macroglobulin isgenetically associated with Alzheimer’s disease. Nature Genet 1998;19: 357–60.59. Wavrant-DeVrieze F, Rudrasingham V, Lambert JC et al. Noassociation between the alpha-2 macroglobulin I1000Vpolymorphism and Alzheimer’s disease. Neurosci Lett 1999; 262:137–9.The Lundby Study, 1947–1997Per Nettelbladt 1 , Olle Hagnell 1 , Leif O¨ jesjo¨2, Lena Otterbeck 1 , Cecilia Mattisson 1 , Mats Bogren 1 ,Erik Hofvendahl 1 , Per Tora˚ker 11 Lund University Hospital and 2 Karolinska Institute, Stockholm, SwedenThe Lundby Study is a prospective, longitudinal investigation of allkinds of mental disorders in a total population. It started in 1947,when four psychiatrists, Essen-Mo¨ller et al., interviewed anddescribed all the 2550 inhabitants of a geographically delimitedarea in southern Sweden. They were interested in finding out howmany people were suffering from a mental illness or deviation, andalso the way normal and abnormal personality traits weredistributed in a normal population. They traced and examined allbut 1% of the population. Only four people refused to participate.After 10 years, in 1957, the field investigation was repeated. Onepsychiatrist alone (Hagnell) re-examined the original populationfrom 1947, irrespective of domicile. For deceased persons,information was collected from hospital case notes and fromrelatives. Hagnell also examined the 1013 newcomers in Lundbyand thus performed a new prevalence study of 2612 people, as wellas a 10 year incidence study of the original 2550 subjects. In 1972Hagnell and O¨jesjo¨ made a second follow-up study 1 including thetotal population of 3563, also this time irrespective of domicile,thus performing a 25 year and a 15 year incidence study. Theparticipation rate was as high as 98% at the two follow-ups.All the three field examinations were performed in a similarway. One part of the examination was a semi-structuredinterview, the other part a free conversation. The task of thepsychiatrist was to collect the information to the best of hisability, observantly looking for symptoms and signs. In aninvestigation such as this, the data should ideally be collectedby a trained psychiatrist. To facilitate his task, the psychiatristhad a structured form to fill in. Each interview turned out to bedifferent, but the information gathered was noted in asystematic way. Supplementary information was collectedfrom, amongst other sources, official registers, hospital casenotes, autopsy reports, social insurance offices, local officialsand relatives. This additional information from other sourcesforms a rich resource and has proved to be particularlyvaluable when evaluating the dementias of the elderly. All thetypes of information collected formed the basis for the globalevaluation and classification.The material from the three field studies has enabled us not onlyto estimate the rates of prevalence, incidence and probability ofdeveloping a mental illness, but also to identify possible backgroundfactors of, for example, dementia, starting with peoplewho were healthy at one investigation but who had contracted theillness before the next. Trying to identify risk factors is a weightyenterprise in which we are still involved.In an epidemiological, psychiatric investigation, precise clinicalclassification tools are hardly applicable. For dementias amongthe elderly we use two diagnostic groups: senile dementia of theAlzheimer type (SDAT) and vascular dementia (MID), the lattercharacterized by focal brain symptoms. Of course, otherdementias of the elderly exist but they are fairly unusualcompared with SDAT and vascular dementia and not very easilyrecognized in epidemiological investigations.In order also to be able to include the hereditary aspect, wehave mapped out the kinship of every proband down to the sixthgeneration, and for the original 2550 even down to the seventhgeneration.From the Lundby Study, several reports on dementias in theelderly have been published. Figures from the 1972 prevalencestudy are included in the EURODEM comparative prevalencestudies 2,3 . For the 10 year age groups 60, 70 and 80, the prevalence

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