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Alzheimer's disease (AD) is the most common neurological disorder associated with ageing and has a global prevalence of 6% in people older than 65 years.1 It is also the most common cause of dementia, accounting for 50%–60% of all cases.2 The increase in life expectancy of the world population is expected to translate into many more cases of dementia—it is estimated that 1 in 85 persons worldwide will be affected by AD in 2050.1 Clearly, AD is a major public health problem.
To examine whether physical activity (PA) may influence the risk of AD requires a brief review of pathogenesis. Risk factors for the disease include advanced age, family history of dementia, low educational accomplishment and presence of the ε4 isoform of the apolipoprotein E (apoE).3 ApoE ε4 has been associated with all the AD-related biochemical disturbances such as β-amyloid deposition, tangle formation, oxidative stress, lipid homeostasis deregulation, synaptic plasticity loss and cholinergic dysfunction.3 Individuals who are homozygotes for the APOE ε4 genotype have up to 15 times higher risk of developing AD compared with non-carriers.4 Further, the median age at AD onset is reduced from 84 years in non-ε4 carriers to 68 years in ε4 homozygotes.5 The presence of APOE ε4 acts in synergy with several lifestyle factors (fat and alcohol intake, smoking and also physical inactivity) to increase the risk for AD.6
Biochemical underpinnings of pa's beneficial effect on ad mechanisms
How does PA influence the biochemical disturbances described above?7/sup> In AD mouse models, 5 months of aerobic exercise delayed β-amyloid accumulation and enhanced the rate of learning.9 PA augmented brain plasticity10 by facilitating regenerative, …
AL and JRR drafted the manuscript and contributed equally.
Competing interests None.
Provenance and peer review Not commissioned; externally peer reviewed.