Transgenic mouse models amyloid plaques

Li G Yang X, Yang E, Dai G. (2010) Coenzyme QIO reduces beta-amyloid plaque in an APP/PSl transgenic mouse model of Alzheimer s disease. JMol Neurosci 41 110-113. 

Schmitz C, Rutten BP, Pielen A, Schafer S, Wirths O, Tremp G, Czech C, Blanchard V, Multhaup G, Rezaie P, Korr H, Steinbusch HW, Pradier L, Bayer TA (2004) Hippocampal neuron loss exceeds amyloid plaque load in a transgenic mouse model of Alzheimer s disease. Am J Pathol 164 1495-1502... 

Frenkel D, Dewachter I, Van Leuven F, Solomon B (2003) Reduction of beta-amyloid plaques in brain of transgenic mouse model of Alzheimer s disease by EFRH-phage immunization. Vaccine 21 1060-1065. 

Transgenic mouse models of AD require two or more mutations to reproduce all the physical features of AD (AB plaques and tau tangles), however these models have not provided any leads to the relationship between AB plaques and tau tangles. Most mouse models of AD are considered limited or incomplete several models develop amyloid deposition but fail to develop neurofibrillary tangles that are an essential hallmark of AD. Neuritic atrophy is found in some transgenics, but of nearly one dozen mouse models, only one has reported loss of neurons that is characteristic of AD (Herrup et ah, 2004). Some tau models develop severe memory deficits associated with AD but express little amyloid protein (Mandavilli, 2006). These shortfalls limit the usefulness of these models for developing therapeutic strategies for AD (Schwab et ah, 2004). 

Nilsson LN, B.K., DiCarlo G, Gordon MN, Morgan D, Paul SM, Potter H., Alpha-1-antichymotrypsin promotes beta-sheet amyloid plaque deposition in a transgenic mouse model of Alzheimer s disease. J Neurosci, 2001.21(5) p. 1444-51. 

Impairment of glucose metabolism is a major feature of Alzheimer s disease. Pan et al. (59) have examined the effect of benfotiamine on cognitive impairment and pathology in the amyloid precursor proteins/presenilin-1 transgenic mice, a mouse model of Alzheimer s disease. Chronic treatment with benfotiamine enhanced the spatial memory of the mice and also reduced both amyloid plaque numbers and phosphorylated tau levels in the cortical areas. Benfotiamine increased the phosphorylation level of glycogen synthase kinase-3a and 3P and reduced their enzyme activities, a newer aspect of the effect of benfotiamine. 

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