Abstract
While the link between amyloid β (Aβ) accumulation and synaptic degradation in Alzheimer's disease (AD) is known, the consequences of this pathology on population coding remain unknown. We found that the entropy, a measure of the diversity of network firing patterns, was lower in the dorsal CA1 region in the APP/PS1 mouse model of Aβ pathology, relative to controls, thereby reducing the population's coding capacity. Our results reveal a network level signature of the deficits Aβ accumulation causes to the computations performed by neural circuits.
Publication types
-
Research Support, N.I.H., Extramural
-
Research Support, Non-U.S. Gov't
-
Research Support, U.S. Gov't, Non-P.H.S.
MeSH terms
-
Alzheimer Disease / genetics
-
Alzheimer Disease / metabolism*
-
Alzheimer Disease / pathology
-
Amyloid beta-Protein Precursor / genetics
-
Amyloid beta-Protein Precursor / metabolism*
-
Animals
-
CA1 Region, Hippocampal / metabolism*
-
CA1 Region, Hippocampal / pathology
-
Disease Models, Animal
-
Female
-
Humans
-
Male
-
Mice
-
Neurons / cytology*
-
Neurons / metabolism
-
Presenilin-1 / genetics
-
Presenilin-1 / metabolism
Substances
-
Amyloid beta-Protein Precursor
-
Presenilin-1