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P3‐024: Hippocampal synaptic plasticity in Alzheimer's disease: what have we learned so far from transgenic models?
Author(s) -
Marchetti Cristina,
Marie Hélène
Publication year - 2011
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2011.05.1463
Subject(s) - neuroscience , long term potentiation , synaptic plasticity , neurotransmission , inhibitory postsynaptic potential , excitatory postsynaptic potential , hippocampal formation , biology , hippocampus , genetically modified mouse , transgene , genetics , receptor , gene
express three mutations: APPswe PS1M146V, and tauP301L Results: Histochemical and immunohistochemical staining combined with computerized stereology of systematically sampled sections from 3xTg mice in three age groups [8, 12, and 15 months] revealed remarkable similarities and differences relative to age-matched dtg APPswe/PS1DE9 mice. While 3xTg mice show significant age-related loss of TH+ neurons in LC, they do not show age-related loss of CA1 neurons as seen in dtg APPswe/PS1DE9 mice. The 3xTg mice have a distinctive pattern of extracellular distribution of amyloid plaques limited primarily to the subiculum of hippocampal formation and neocortical layer Vand intracellular Aß deposition primarily in subiculum and CA1 pyramidal neurons. Furthermore, significant differences were found in the degree of astrogliosis and microgliosis in dtg APPswe/PS1DE9 and 3xTg mice.Conclusions:Understanding the neurobiological bases for these similarities and differences in AD-type neuropathology in response to the deposition of mutant Aß peptides could provide insight into neuropathology underlying cognitive impairment in AD.