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Hypoxic conditions in severely anemic individuals may cause brain damage resulting in cognitive impairment. [32] When iron levels in the brain are disrupted neurophysiological mechanisms and cognition are affected, potentially resulting in long-term behavioral changes and may affect attention span, intelligence, sensory perception functions ...
The blood–brain barrier is formed by the brain capillary endothelium and excludes from the brain 100% of large-molecule neurotherapeutics and more than 98% of all small-molecule drugs. [28] Overcoming the difficulty of delivering therapeutic agents to specific regions of the brain presents a major challenge to treatment of most brain disorders.
Replacing red meat with plant-based protein sources such as nuts and legumes was associated with a 19% lower risk of dementia and 1.37 fewer years of cognitive aging, according to the study.
Help protect your brain against cognitive decline, memory loss, cell damage, and more with these 14 foods. ... It’s a plant-based source of the brain-boosting DHA omega-3 fatty acid. It’s also ...
The blood–brain barrier is formed by special tight junctions between endothelial cells lining brain blood vessels. Blood vessels of all tissues contain this monolayer of endothelial cells, however only brain endothelial cells have tight junctions preventing passive diffusion of most substances into the brain tissue. [1]
Areas of the brain such as the insula [44] and anterior circulate cortex (ACC) have been found to be disturbed in individuals with BN. [45] These areas are involved in self-regulation as well as executive control which controls cognitive processes including working memory, and may be the reason for impairment.
A further consequence of damage to the endothelium is the release of pathological quantities of von Willebrand factor, which promote platelet aggregation and adhesion to the subendothelium, and thus the formation of potentially fatal thrombi. Angiosarcoma is cancer of the endothelium and is rare with only 300 cases per year in the US. [29]
The GLUT1 protein that transports glucose across the blood brain barrier is encoded by the SLC2A1 gene, located on chromosome 1. [8] In GLUT1 deficiency syndrome, one of the two genes is damaged by a mutation and an insufficient amount protein is made. As a result, insufficient glucose is passing the blood brain barrier.