Vascular Effects on Cerebrovascular Permeability and Neurodegeneration

Neurons and glial cells in the brain are protected by the blood brain barrier (BBB). The local regulation of blood flow is determined by neurons and signal conducting cells called astrocytes. Although alterations in neurons and glial cells affect the function of neurons, the majority of effects are coming from other cells and organs of the body. Although it seems obvious that effects beginning in brain vasculature would play an important role in the development of various neuroinflammatory and neurodegenerative pathologies, significant interest has only been directed to the possible mechanisms involved in the development of vascular cognitive impairment and dementia (VCID) for the last decade. Presently, the National Institute of Neurological Disorders and Stroke applies considerable attention toward research related to VCID and vascular impairments during Alzheimer's disease. Thus, any changes in cerebral vessels, such as in blood flow, thrombogenesis, permeability, or others, which affect the proper vasculo-neuronal connection and interaction and result in neuronal degeneration that leads to memory decline should be considered as a subject of investigation under the VCID category. Out of several vascular effects that can trigger neurodegeneration, changes in cerebrovascular permeability seem to result in the most devastating effects. The present review emphasizes the importance of changes in the BBB and possible mechanisms primarily involving fibrinogen in the development and/or progression of neuroinflammatory and neurodegenerative diseases resulting in memory decline.

Automated summary

Neurons and glial cells in the brain are protected by the blood brain barrier (BBB). Local regulation of blood flow in the brain is determined by neurons and astrocytes. Changes in cerebral vessels, particularly in cerebrovascular permeability, play a crucial role in the development and progression of neuroinflammatory and neurodegenerative diseases, resulting in memory decline.