Treadmill Exercise Prevents Learning and Memory Impairment in Alzheimer’s Disease-Like Pathology

An T.      Dao; Munder A.      Zagaar; Amber T.      Levine; Samina      Salim; Jason L.      Eriksen; Karim A.      Alkadhi

doi:10.2174/1567205011310050006

Abstract

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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