So you described a problem but offered NO SOLUTION, what the fuck good does that do?
Brain injury-induced dysfunction of the blood brain barrier as a risk for dementia
Abstract
The
blood-brain barrier (BBB) is a complex and dynamic physiological
interface between brain parenchyma and cerebral vasculature. It is
composed of closely interacting cells and signaling molecules that
regulate movement of solutes, ions, nutrients, macromolecules, and
immune cells into the brain and removal of products of normal and
abnormal brain cell metabolism. Dysfunction of multiple components of
the BBB occurs in aging, inflammatory diseases, traumatic brain injury
(TBI, severe or mild repetitive), and in chronic degenerative dementing
disorders for which aging, inflammation, and TBI are considered risk
factors. BBB permeability changes after TBI result in leakage of serum
proteins, influx of immune cells, perivascular inflammation, as well as
impairment of efflux transporter systems and accumulation of
aggregation-prone molecules involved in hallmark pathologies of
neurodegenerative diseases with dementia. In addition, cerebral vascular
dysfunction with persistent alterations in cerebral blood flow and
neurovascular coupling contribute to brain ischemia, neuronal
degeneration, and synaptic dysfunction. While the idea of TBI as a risk
factor for dementia is supported by many shared pathological features,
it remains a hypothesis that needs further testing in experimental
models and in human studies. The current review focusses on pathological
mechanisms shared between TBI and neurodegenerative disorders
characterized by accumulation of pathological protein aggregates, such
as Alzheimer's disease and chronic traumatic encephalopathy. We discuss
critical knowledge gaps in the field that need to be explored to clarify
the relationship between TBI and risk for dementia and emphasize the
need for longitudinal in vivo studies using imaging and biomarkers of
BBB dysfunction in people with single or multiple TBI.
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