Exercise Is More Effective than Diet Control in Preventing High Fat Diet-induced β-Amyloid Deposition and Memory Deficit in Amyloid Precursor Protein Transgenic Mice

Abstract

Background: Exercise and diet control are fundamental approaches to metabolic conditions caused by high fat diet (HFD). Results: HFD-induced memory deficit and A␤ deposition were more ameliorated in the exercise-than in the diet controlinduced mice. Conclusion: Exercise was more effective than diet control in preventing HFD-induced AD development. Significance: Exercise has the highest priority in the prevention of AD.

Prevention of Cognitive Decline in Later Life

“…Recent reports also suggested that exercise may have a direct impact on AD pathology. In mice models for AD and Parkinson's disease, there have been evidence that exercise enhanced production of neurotrophic factors, attenuate the deposition of Aß42 protein and improved mitochondrial function (Lau, Patki, Das-Panja, Le, & Ahmad, 2011;Maesako et al, 2012). There are also reports indicating enhanced brain network connectivity and larger brain volumes in the aerobic exercise, and social intervention groups, suggesting a brain modulating response to life style interventions (Ahlskog, Geda, Graff-Radford, & Petersen, 2011;Mortimer et al, 2012).…”

Are microRNAs the Molecular Link Between Metabolic Syndrome and Alzheimer’s Disease?

“…It has been clearly established in controlled studies that regular vigorous exercise improves mood and cognition [194]. In fact, voluntary exercise ameliorates HFD-induced memory deficits and Aβ deposition in APP transgenic mice [195]. It has been established that part of the beneficial effects of exercise in skeletal muscle is attributed to miRNA regulation [196]; however, the evidence of miRNA responsive to exercise in brain is scarce.…”

Is physical activity an Elixir?

“…A testedzés továbbá képes az oxidatív sérülést javító enzimrendszerek aktiválására [41], és az úgynevezett "housekeeping" enzimek, mint például a proteaszóma, aktivitását serkenteni, amely szerepet játszhat az oxidatív sérülés csökkenésében [40,42]. Ide kapcsolódhat az is, hogy a testedzés képes a neprilysin és az inzulinbontó enzim aktivitását emelni, ami azért fontos, mert ezek az enzimek bontják a béta-amyloidot, amelynek a felszaporodása oka és velejárója az Alzheimer-betegségnek [32,43]. A testedzés ezenkívül a felfokozott keringésen keresztül jelentősen javítja az agy vérellátását és serkenti új erek képződését is [44], amely szerepet játszhat az agy anyagcsere-folyamatainak a szabályozásá-ban is [45].…”