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Genes for Alzheimer Dementia

  • J. Theuns and C. Van Broeckhoven
Extract

Alzheimer disease (AD), the most common form of dementia in the elderly, is rapidly becoming a major health problem in developed countries where the number of elderly people continuously grows due to improved medical care. Consequently, the number of AD patients is increasing and thus far no effective therapies are available. Clinically the disease can be diagnosed with 90% reliability on the basis of neurological examination, neuropsychological testing and brain imaging techniques. A definite diagnosis, however, requires the post-mortem detection of senile plaques (SPs) and neurofibrillary tangles (NFTs) in the brain. The SPs are extracellular deposits mainly composed of amyloid P (Ap) surrounded by dystrophic neurites. NFT are intraneural inclusions of paired helical filaments composed of hyperphosphorylated tau.

Although age is the major risk factor for AD, population survey and family studies have provided substantial evidence that genetic factors are major contributors to the expression of AD.

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Corresponding author
Laboratory of Neurogenetics, University of Antwerp (UIA), Department of Biochemistry, Universiteitsplein 1, B-2610 Antwerpen, Belgium
References
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1.De Jonghe, C. Van Broeckhoven, C. Identification and functional Analysis of Genes and genetic Risk Factors in Alzheimer's Disease. In: Molecular-Genetic Techniques for Behavioural Neurosciences. Crusio, WE, Gerlai, R, eds. Amsterdam: Elsevier, 1999; in press
2.Van Broeckhoven, CL. Molecular genetics of Alzheimer disease: identification of genes and gene mutations. Eur Neurol 1995; 35:819.
3.Duijn, CM van, Clayton, DG, Chandra, V, et al.Interaction between genetic and environmental risk factors for Alzheimer's disease: a reanalysis of case-control studies. EURODEM Risk Factors Research Group. Genet Epidemiol 1994; 11: 539–51.
4.Goate, A, Chartier-Harlin, MC, Mullan, M, et al.Segregation of a missense mutation in the amyloid precursor protein gene with familial Alzheimer's disease. Nature 1991; 349: 704–6.
5.Sherrington, R, Rogaev, EI, Liang, Y, et al.Cloning of a gene bearing missense mutations in early-onset familial Alzheimer's disease. Nature 1995; 375: 754–60.
6.Theuns, J, Cruts, M, Del-Favero, J, et al.Determination of the genomic organization of human presenilin 1 by fiber-FISH analysis and restriction mapping of cloned DNA. Mamm Genome 1999; 10: 410–4.
7.Cruts, M, Van Broeckhoven, C. Molecular genetics of Alzheimer's disease. Ann Med 1998; 30: 560–5.
8.Levy-Lahad, E, Wasco, W, Poorkaj, P, et al.Candidate gene for the chromosome 1 familial Alzheimer's disease locus. Science 1995; 269: 973–7.
9.Pericak-Vance, MA, Bebout, JL, Gaskell-PC, J, et al.Linkage studies in familial Alzheimer disease: evidence for chromosome 19 linkage. Am J hum Gen 1991; 48: 1034–50.
10.Pericak-Vance, MA, Bass, MP, Yamaoka, LH, et al.Complete genomic screen in late-onset familial Alzheimer disease. Evidence for a new locus on chromosome 12. JAMA 1997; 278,1237–41.
11.Van Broeckhoven, C. Alzheimer's disease: identification of genes and genetic risk factors. Prog Brain Res 1998;117;315–25.
12.Wragg, M, Hutton, M, Talbot, C. Genetic association between intronic polymorphism in presenilin-1 gene and late-onset Alzheimer's disease. Alzheimer's Disease Collaborative Group. Lancet 1996;347;509–12.
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Acta Neuropsychiatrica
  • ISSN: 0924-2708
  • EISSN: 1601-5215
  • URL: /core/journals/acta-neuropsychiatrica
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