Nearly 100 years ago, a group of Bavarian psychiatrists gatheredin a small conference hall in Tübingen to hear a presentationby Dr. Alois Alzheimer. To their surprise, he proposed thatpresenile dementia in his 51-year-old patient might be relatedto two brain lesions he referred to as "miliary bodies" lyingoutside of neurons and "dense bundles of fibrils" choking theinteriors of neurons. Today, we consider these lesions to bethe neuropathological hallmarks of the disease that is namedafter him and refer to them as senile plaques and neurofibrillarytangles, respectively. Although abundant levels of these brainlesions . . . [Full Text of this Article]
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From the Genetics and Aging Research Unit, Massachusetts General Hospital and Harvard Medical School, Charlestown, Mass.
Utsuki, T., Uchimura, N., Irikura, M., Moriuchi, H., Holloway, H. W., Yu, Q.-S., Spangler, E. L., Mamczarz, J., Ingram, D. K., Irie, T., Greig, N. H.
(2007). Preclinical Investigation of the Topical Administration of Phenserine: Transdermal Flux, Cholinesterase Inhibition, and Cognitive Efficacy. J. Pharmacol. Exp. Ther.
321: 353-361
[Abstract][Full Text]
King, M. E., Kan, H.-M., Baas, P. W., Erisir, A., Glabe, C. G., Bloom, G. S.
(2006). Tau-dependent microtubule disassembly initiated by prefibrillar {beta}-amyloid. JCB
175: 541-546
[Abstract][Full Text]
Mendez, M. F., McMurtray, A.
(2006). Frontotemporal dementia-like phenotypes associated with presenilin-1 mutations.. AM J ALZHEIMERS DIS OTHER DEMEN
21: 281-286
[Abstract]
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