By Hooper N.M. (ed.)
This article brings jointly the most options of biochemistry, mobilephone biology, and molecular biology which are getting used to enquire the molecular foundation of Alzheimer's illness. It offers a precis of at the moment on hand healing brokers and customers for destiny medicines.
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R. (1988) Dementia: characteristics of a referral population and factors associated with progression. Neurology 38, 1083–1090. 5. , Tanja, T. , et al. (1989) History of dementia and Parkinson’s disease in first degree relatives of patients with Alzheimer’s disease. Neurology 39, 1589–1592. 6. Hoininen, H. and Heinonen, O. P. (1982) Clinical and etiological aspests of senile dementia. Eur. Neurol. 21, 401–410. 7. , Wilkinson, W. , Stafford, J. , Helms, M. , Sigmon, A. , and Weinberg, T. (1984) Alzheimer’s disease: a study of epidemiological aspects.
Et al. (1997) No association between the very-low density lipoprotein receptor gene and late-onset Alzheimer’s disease, nor interaction with apolipoprotein E gene in population based and clinic samples. Genet. Epidem. 14, 299–205. 86. , Ng, H. , Chan, Y. , Mak, Y. , et al. (1998) No association detected between the very low density lipoprotein receptor (VLDL-R) and late onset Alzheimer’s disease in Hong Kong Chinese. Neurosci. Lett. 241, 33–36. 87. , et al. (1997) Lack of association of the very-low density lipoprotein receptor gene polymorphism with Caucasian 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.