[The role of Alzheimer amyloid plaques in the mechanisms of neuron synaptic plasticity disturbance].
The authors studied hippocampal microscopic sections taken from transgenic mice expressing non-mutated human amyloid precursor protein (APP695), and age-matched non-transgenic control mice. The aim of the study was to reveal individual effects of plaque-like amyloid of aged (25.5 months) transgenic mice and diffuse amyloid of non-transgenic mice (verified by immunohistochemistry and Congo Red fluorescence) on synaptic plasticity. In vitro extracellular recording of excitatory postsynaptic potentials from hyppocampal CA1 area revealed impairment of input/output characteristics and long-term potentiation, and a several-millisecond delay of initial post-tetanic traces in aged transgenic vs. control mice. The results show that amyloid plaques (not diffuse amyloid) may be one of the causes of synaptic dysfunction in Alzheimer disease.
Berezov
T T
TT
Kudinova
N V
NV
Kudinov
A P
AP
D000544:Alzheimer Disease / Q000378:metabolism* / Q000503:physiopathology*; D016564:Amyloid beta-Protein Precursor / Q000378:metabolism*; D000818:Animals; D004195:Disease Models, Animal; D006624:Hippocampus / Q000378:metabolism / Q000473:pathology; D007150:Immunohistochemistry; D051379:Mice; D009473:Neuronal Plasticity / Q000502:physiology*; D058225:Plaque, Amyloid / Q000378:metabolism*; D009435:Synaptic Transmission / Q000502:physiology*
D016564:Amyloid beta-Protein Precursor