Cerebral hemodynamics of the aging brain: risk of Alzheimer disease and benefit of aerobic exercise

Takashi Tarumi,Rong Zhang

doi:10.3389/fphys.2014.00006

Abstract

Alzheimer disease (AD) and cerebrovascular disease often coexist with advanced age. Mounting evidence indicates that the presence of vascular disease and its risk factors increase the risk of AD, suggesting a potential overlap of the underlying pathophysiological mechanisms. In particular, atherosclerosis, endothelial dysfunction, and stiffening of central elastic arteries have been shown to associate with AD. Currently, there are no effective treatments for the cure and prevention of AD. Vascular risk factors are modifiable via either pharmacological or lifestyle intervention. In this regard, habitual aerobic exercise is increasingly recognized for its benefits on brain structure and cognitive function. Considering the well-established benefits of regular aerobic exercise on vascular health, exercise-related improvements in brain structure and cognitive function may be mediated by vascular adaptations. In this review, we will present the current evidence for the physiological mechanisms by which vascular health alters the structural and functional integrity of the aging brain and how improvements in vascular health, via regular aerobic exercise, potentially benefits cognitive function.

Highlights

Alzheimer’s disease (AD) is a devastating neurological disorder characterized by progressive deterioration of brain structure and function (Querfurth and LaFerla, 2010)
SUMMARY AD and cerebrovascular disease often coexist in the aging brain
Traditional view that AD and vascular dementia (VaD) are two divergent clinical entities with few or no overlap between their pathologies is challenged by an accumulating body of evidence indicating a close association between vascular disease and the risk of AD development

Summary

Introduction

Alzheimer’s disease (AD) is a devastating neurological disorder characterized by progressive deterioration of brain structure and function (Querfurth and LaFerla, 2010). Mounting evidence indicates that vascular disease and risk factors elevate the risk of vascular dementia (VaD) and AD (de la Torre, 2004). VaD is attributed to cerebral hypoperfusion and ischemia that are associated with impairment of synaptic activity and protein synthesis, glutamate excitotoxicity, and neuronal apoptosis (Hossmann, 1994; Gorelick et al, 2011). Despite these traditional perspectives, large populationbased prospective studies have demonstrated that vascular risk factors in midlife, such as systolic hypertension and hyperlipidemia, led to a significant elevation of AD risk in later life (Kivipelto et al, 2001)

Objectives

Conclusion