Read e-book online Alzheimer's disease and related disorders annual, 2002 PDF

By Jeffrey L Cummings, Serge Gauthier

ISBN-10: 1841842346

ISBN-13: 9781841842349

Given the improvement of recent healing thoughts and items, Serge Gauthier and Jeffrey Cummings have compiled an inventory of latest themes with a purpose to be of curiosity basically to neurologists targeting Alzheimer's disorder, and likewise to psychiatrists and geriatricians. The participants, all revered of their subspecialties, have written up to date, comprehensively referenced chapters which should supply assistance in addition to stimulate dialogue on the place present remedy is heading.

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Extra resources for Alzheimer's disease and related disorders annual, 2002

Sample text

Neuroreport 1995; 6:489–492. 96. Hensley K, Butterfield DA, Mattson M et al. A model for beta-amyloid aggregation and neurotoxicity based on the free radical generating capacity of the peptide: implications of ‘molecular shrapnel’ for Alzheimer’s disease. Proc West Pharmacol Soc 1995; 38:113–120. 97. Chen Y, McPhie DL, Hirschberg J, Neve RL. The amyloid precursor protein-binding protein APP-BP1 drives the cell cycle through the SM checkpoint and causes apoptosis in neurons. J Biol Chem 2000; 275:8929–8935.

Cullen WK, Suh YH, Anwyl R, Rowan MJ. Block of LTP in rat hippocampus in vivo by beta-amyloid precursor protein fragments. Neuroreport 1997; 8:3213–3217. 59. Freir DB, Holscher C, Herron CE. Blockade of long-term potentiation by beta-amyloid peptides in the CA1 region of the rat hippocampus in vivo. J Neurophysiol 2001; 85:708–713. 60. Itoh A, Akaike T, Sokabe M et al. Impairments of long-term potentiation in hippocampal slices of beta-amyloid-infused rats. Eur J Pharmacol 1999; 382:167–175. 61.

The cell cycle molecules such as the cyclin-dependent kinases are also attractive targets for therapy. Therapies could also be directed directly against the caspases using broad or narrow spectrum inhibitors. This might allow neurons under attack to hang on a bit longer. It might also maintain totally nonfunctional neurons on life support at the expense of healthier cells in the brain. Conclusion In summary, it is likely that apoptosis in AD results from a variety of causes. An understanding or the pathways leading to apoptosis can suggest a variety of therapeutic targets which might stop the damage long before the cell is mortally wounded.

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Alzheimer's disease and related disorders annual, 2002 by Jeffrey L Cummings, Serge Gauthier

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