Parvalbumin neuroplasticity compensates for somatostatin impairment, maintaining cognitive function in Alzheimer's disease.

ABSTRACT:

Background

Patient-to-patient variability in the degree to which β-amyloid, tau and neurodegeneration impact cognitive decline in Alzheimer's disease (AD) complicates disease modeling and treatment. However, the underlying mechanisms leading to cognitive resilience are not resolved. We hypothesize that the variability in cognitive function and loss relates to neuronal resilience of the hippocampal GABAergic network.

Methods

We compared TgF344-AD and non-transgenic littermate rats at 9, 12, and 15 months of age. Neurons, β-amyloid plaques and tau inclusions were quantified in hippocampus and entorhinal cortex. Somatostatin (SST) and parvalbumin (PVB) interneurons were traced to examine hippocampal neuroplasticity and cognition was tested in the Barnes maze.

Results

The

SUBMITTER: Morrone CD 

PROVIDER: S-EPMC9063209 | biostudies-literature | 2022 May

REPOSITORIES: biostudies-literature