Alzheimer’s disease (AD) is a neurodegenerative disorder that is characterized by progressive memory loss. In
contrast, accumulating evidence suggests a neuroprotective role of regular exercise in aging associated memory impairment.
In this study, we investigated the ability of regular exercise to prevent impairments of short-term memory (STM)
and early long-term potentiation (E-LTP) in area CA1 of the hippocampus in a rat model of AD (i.c.v. infusion of 250
pmol/day Aβ1-42 peptides). We utilized behavioral assessment, in vivo electrophysiological recording, and immunoblotting
in 4 groups of adult Wistar rats: control, treadmill exercise (Ex), β-amyloid-infused (Aβ), and amyloid-infused/treadmill
exercised (Ex/Aβ). Our findings indicated that Aβ rats made significantly more errors in the radial arm water maze
(RAWM) compared to all other groups and exhibited suppressed E-LTP in area CA1, which correlated with deleterious
alterations in the levels of memory and E-LTP-related signaling molecules including calcineurin (PP2B), brain derivedneurotrophic
factor (BDNF) and phosphorylated CaMKII (p-CaMKII). Compared to controls, Ex and Ex/Aβ rats showed
a similar behavioral performance and a normal E-LTP with no detrimental changes in the levels of PP2B, BDNF, and p-
CaMKII. We conclude that treadmill exercise maybe able to prevent cognitive impairment associated with AD pathology.
Keywords: Alzheimer’s disease, brain-derived neurotrophic factor (BDNF), calcineurin (PP2B), calcium-calmodulin dependent
protein kinase II (CaMKII), exercise, learning and memory, synaptic plasticity.
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