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By Suzanne De La Monte

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Extra resources for Alzheimer’s Disease Pathogenesis-Core Concepts, Shifting Paradigms and Therapeutic Targets

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Amyloid plaques and NFT result from an aberration in deposition of the Aβ peptide and the hyperphosphorylated tau protein, respectively, and these depositions lead to neuronal loss and neurotoxicity in the brain affected by AD (Isik, 2010). However, plaques and NFTs are not unique to AD, as these same structural changes occur with normal aging and in many others neurodegenerative disorders (Jackson-Siegal, 2005). Great confusion existed as to whether the dementia often observed in normal aging and AD were the same or different entities.

Some authors hypothesize that the clinical expresion of depression needs some indemnity of cholinergic pathways, close to normal levels, which occurs only in initial stages. As mentioned before, there is evidence of early changes in regional CBF, which could be related to the degeneration of cholinergic population that has a regulatory effect. This is known as the cholinergic-vascular theory. As part of a research project in our institution (International Center of Neurological Restauration-CIREN), and with the collaboration of other Cubans institutions, we compared the global cerebral blood flow (gCBF) in absolute units (ml/min/100 g) at resting state 16 Alzheimer’s Disease Pathogenesis-Core Concepts, Shifting Paradigms and Therapeutic Targets between 38 controls and 40 amnestic MCI subjects, both groups with similar demographic and vascular risk factors (limited).

365375. , C. M. Lill, and R. E. Tanzi, 2010, The genetics of Alzheimer disease: back to the future: Neuron, v. 68, no. 2, p. 270-281. Bowman, G. , J. A. Kaye, M. Moore, D. Waichunas, N. E. Carlson, and J. F. Quinn, 2007, Blood-brain barrier impairment in Alzheimer disease: stability and functional significance: Neurology, v. 68, no. 21, p. 1809-1814. Chen, D. , S. A. Stern, A. Garcia-Osta, B. Saunier-Rebori, G. Pollonini, D. BambahMukku, R. D. Blitzer, and C. M. Alberini, 2011, A critical role for IGF-II in memory consolidation and enhancement: Nature, v.

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