Interactions between glial cells and the blood-brain barrier and their role in Alzheimer's disease

Oct 5, 2021Ageing research reviews

How support cells and the brain’s protective barrier interact in Alzheimer's disease

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Abstract

Dysfunction of the blood-brain barrier (BBB) may play a significant role in the onset and progression of Alzheimer’s disease (AD).

Alzheimer's disease is characterized by irreversible neurodegeneration, with senile plaques and neurofibrillary tangles being common features.
Currently, no effective curative therapies exist for Alzheimer's disease.
The blood-brain barrier serves as a selective barrier that helps maintain brain homeostasis.
Injury to the blood-brain barrier could contribute to Alzheimer’s disease pathogenesis, though the exact mechanisms remain unclear.
Glial cells are suggested to play a crucial role in maintaining the integrity of the blood-brain barrier and supporting neuronal function.

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Alzheimer's disease (AD), which is an irreversible neurodegenerative disorder characterized by senile plaques and neurofibrillary tangles, is the most common form of dementia worldwide. However, currently, there are no satisfying curative therapies for AD. The blood-brain barrier (BBB) acts as a selective physical barrier and plays protective roles in maintaining brain homeostasis. BBB dysfunction as an upstream or downstream event promotes the onset and progression of AD. Moreover, the pathogenesis of AD caused by BBB injury hasn't been well elucidated. Glial cells, BBB compartments and neurons form a minimal functional unit called the neurovascular unit (NVU). Emerging evidence suggests that glial cells are regulators in maintaining the BBB integrity and neuronal function. Illustrating the regulatory mechanism of glial cells in the BBB assists us in drawing a glial-vascular coupling diagram of AD, which may offer new insight into the pathogenesis of AD and early intervention strategies for AD. This review aims to summarize our current knowledge of glial-BBB interactions and their pathological implications in AD and to provide new therapeutic potentials for future investigations.

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Abstract

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