About this Research Topic
The thematic issue “BBB dysfunction in the aging brain” will cover recent achievements in deciphering molecular mechanisms underlying impairment of the blood-brain barrier (BBB) in aging. It is well known that age-related neurodegeneration is associated with prominent changes in BBB permeability, alterations in BBB structural and functional integrity, and aberrant activities within the neurovascular unit (NVU). These events are closely related to endothelial dysfunction in cerebral microvessels, deregulation of endothelial-pericyte-astroglial communications, changes in neuronal excitability and glia-controlled support of neuronal activity in the NVU, deregulation of angiogenesis, and loss of regenerative potential of brain cells contributing to NVU/BBB establishment. Above-mentioned mechanisms might serve as a basis for maintaining long-lasting neuroinflammation, progressive cognitive decline and memory impairment, and for ineffective or incorrect action of drugs whose action requires overcoming the BBB.
Recently, it became clear that physiological aging and pathological neurodegeneration, i.e. seen in Alzheimer’s disease or in Parkinson’s disease, could have some significant distinctions in the context of BBB impairment. Thus, it is very timely and important to specify the most prominent changes in the NVU/BBB that are characteristic for normal brain aging and neurodegeneration triggered by pathological stimuli. Therefore, this Research Topic might be organized along the following topics:
i) BBB structure and functions: ontogenesis-related changes;
ii) molecular mechanisms of NVU/BBB impairment in physiological aging;
iii) molecular mechanisms of NVU/BBB impairment in neurodegeneration (with the focus on Alzheimer or Parkinson types of neurodegeneration);
iv) glia-mediated BBB (dys)function and neuroinflammation in aging brain;
v) endothelial dysfunction and cerebral vasculopathy in aging brain;
vi) current approaches to control and monitor BBB permeability in aging brain;
vii) concluding remarks.
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