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Treadmill Exercise Decreases Aβ Deposition and Counteracts Cognitive Decline in APP/PS1 Mice, Possibly via

Xianliang Zhang1, Qiang He2, Tao Huang3

  • 1Shandong University, Jinan, China.

Frontiers in Aging Neuroscience
|April 27, 2019
PubMed

Insights

Treadmill exercise improved cognitive function and reduced Alzheimer's disease pathology in mice. This was achieved by decreasing neuroinflammation and oxidative stress, potentially offering a preventative strategy.

Area of Science:

  • Neuroscience
  • Exercise Physiology
  • Molecular Biology

Background:

  • Alzheimer's disease (AD) is a progressive neurodegenerative disorder.
  • Microglia-mediated neuroinflammation and oxidative stress are implicated in AD pathogenesis.
  • The precise mechanisms by which exercise impacts AD progression remain unclear.

Purpose of the Study:

  • To investigate the effects of treadmill exercise on amyloid-β (Aβ) deposition, cognitive function, and neuroinflammation in a mouse model of early Alzheimer's disease.
  • To analyze the role of microglia polarization and oxidative stress in mediating the benefits of exercise.

Main Methods:

  • Amyloid precursor protein (APP)/PS1 mice were subjected to 12 weeks of treadmill exercise.
  • Cognitive function was assessed using hippocampal-dependent memory tests.
  • Hippocampal tissues were analyzed for Aβ deposition, pro- and anti-inflammatory factors, microglia phenotype (M1/M2), and oxidative stress markers (MDA, SOD, Mn-SOD).

Main Results:

  • Treadmill exercise preserved hippocampal cognitive function in APP/PS1 mice.
  • Exercise significantly suppressed Aβ accumulation in the hippocampus.
  • Neuroinflammation was inhibited, evidenced by reduced pro-inflammatory factors and increased anti-inflammatory mediators, linked to a shift from M1 to M2 microglia phenotype.
  • Oxidative stress was attenuated, with decreased MDA levels and increased SOD and Mn-SOD activities.

Conclusions:

  • Treadmill exercise demonstrates potential therapeutic benefits for early-stage Alzheimer's disease.
  • Exercise may prevent cognitive decline and reduce Aβ pathology by modulating microglia-mediated neuroinflammation and oxidative stress.
  • These findings highlight exercise as a viable non-pharmacological intervention for Alzheimer's disease.
Keywords:
Alzheimer’s diseaseamyloid-βcognitive functionmicroglianeuroinflammationoxidative stresstreadmill exercise

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