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Published on: November 6, 2017
Contributions of vascular ageing to late-onset Alzheimer's disease
Skylyn J Ferguson1, Young Deanna Choi1, Ashley E Walker1
1Department of Human Physiology, University of Oregon, Eugene, Oregon, USA.
Insights
Vascular aging significantly contributes to late-onset Alzheimer's disease (LOAD) by impairing brain blood flow and the blood-brain barrier. Understanding these vascular changes is crucial for developing effective LOAD treatments.
Area of Science:
- Neuroscience
- Gerontology
- Cardiovascular Research
Background:
- Late-onset Alzheimer's disease (LOAD) is linked to vascular risk factors and cerebrovascular issues.
- Aging impacts cerebral blood flow, neurovascular coupling, and blood-brain barrier permeability, potentially initiating LOAD neuropathology.
- Systemic vascular changes like hypertension and arterial stiffness may drive age-related cerebrovascular impairments.
Purpose of the Study:
- To review the evidence linking vascular aging to LOAD.
- To describe age-related cerebrovascular impairments and their underlying causes.
Main Methods:
- Literature review synthesizing current research on vascular aging and LOAD.
Main Results:
- Aging dysregulates cerebral blood flow and neurovascular coupling.
- Increased blood-brain barrier permeability is a hallmark of vascular aging.
- Systemic vascular aging contributes to cerebrovascular impairments.
- Oxidative stress, inflammation, and LOAD pathologies like amyloid-β and tau impair cerebrovascular cells.
Conclusions:
- Vascular aging is a significant contributor to LOAD.
- Age-related cerebrovascular impairments are multifactorial, involving systemic and central vascular changes.
- Further research into these mechanisms is needed for LOAD prevention and treatment.
Abstract:
Late-onset Alzheimer's disease (LOAD) is an age-related disease that is strongly associated with vascular risk factors and cerebrovascular impairments. As such, changes in the vasculature with advancing age likely contribute to LOAD, but the mechanisms underlying these contributions remain incompletely understood. With advancing age, there is dysregulation of cerebral blood flow, impairment of neurovascular coupling, and increased blood-brain barrier permeability, which may initiate or contribute to the neuropathology associated with LOAD. Changes to the vasculature outside of the brain, including increases in blood pressure and arterial stiffness, may initiate age-related cerebrovascular impairments. Age-related increases in oxidative stress and inflammatory signalling, as well as contributions to LOAD-related neuropathology, such as amyloid-β and hyperphosphorylated tau, impair cerebrovascular cells. In this review, we summarize the evidence for the role of vascular ageing in LOAD, describing age-related cerebrovascular impairments and their causes.
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