By Hooper N.M. (ed.)
This article brings jointly the most thoughts of biochemistry, phone biology, and molecular biology which are getting used to enquire the molecular foundation of Alzheimer's affliction. It offers a precis of at present to be had healing brokers and clients for destiny medicines.
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Extra info for Alzheimer's Disease
Lax exclusion criteria may allow a sponsor to claim greater generalizability of their results, while more restrictive exclusion criteria may allow a sponsor to seek higher study completion rate. In one study of a cholinesterase inhibitor, lax exclusion criteria are thought to have resulted in a rate of decline in the placebo group that exceeded most other comparable studies (with more stringent entry criteria). However, it is not clear whether these speculations actually are causally related to entry criteria.
Mutations and polymorphisms in four different genes have now been shown to be either causative or associated with the onset of AD. Mutations in PS-1, PS-2, and APP directly cause the disease with very close to 100% penetrance. Inheritance of the ε4 allele of the ApoE gene is associated with an increased risk of developing AD but is not sufficient to cause the disease. It is evident that the neurodegeneration associated with AD involves a complex system of cellular and molecular interactions, including components of the inflammatory response, the complement system, excitotoxic and oxidative damage etc.
JAMA 278, 1237–1241. , Song, Y. , et al. (1998) Evidence for an Alzheimer disease susceptibility locus on chromosome 12 and for further locus heterogeneity. JAMA 280, 614–618 Wu, W. , et al. (1998) Genetic studies on chromosome 12 in late-onset Alzheimer disease. JAMA 280, 619–622. Pericak-Vance, M. , Bass, M. , Yamaoka, L. , Gaskell P. , Scott, W. , Terwedow, H. , et al. (1991) Linkage studies in familial Alzheimer’s diseaseevidence for chromosome 19 linkage. Am. J. Hum. Genet. 48, 1034–1050. Strittmatter, W.
Alzheimer's Disease by Hooper N.M. (ed.)