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Researchers have shown for the first time in living patients that neuroinflammation - or the activation of immune cells (called microglia) that reside in the brain - is not just the result of disease progression; on the contrary, it is indispensable for disease development.
The key upstream mechanism is missing
.
"In my native Brazil, as a young inpatient neurologist, I noticed that many patients with Alzheimer's disease were neglected and did not receive proper care," said Pete's assistant professor of psychiatry and neurology, MD, Lead author Tharick Pascoal said
.
"Our research shows that combination treatments aimed at reducing amyloid plaque formation and limiting neuroinflammation may be more effective than treating each pathology alone
Alzheimer's disease is characterized by the accumulation of amyloid plaques-protein aggregates between nerve cells in the brain-and disordered clumps of protein fibers formed inside nerve cells called tau tangles
.
Although studies on cultured cells and laboratory animals have accumulated a lot of evidence that the activation of microglia can lead to the spread of tau fibers in Alzheimer's disease, this process has never been confirmed in humans
Research results indicate that targeting neuroinflammation may be beneficial to patients with early Alzheimer's disease.
It may help reverse or at least slow down the accumulation of pathological tau protein in the brain, thereby avoiding dementia
.
In order to determine the mechanism by which disordered tangles of tau protein fibers and amyloid plaques spread in the brain and lead to dementia, the researchers used real-time imaging technology to deeply study the brains of patients with Alzheimer's disease and healthy elderly people at different stages.
.
Researchers have found that neuroinflammation is more common in the elderly and more pronounced in patients with mild cognitive impairment and Alzheimer's disease-related dementia
.
Bioinformatics analysis confirmed that the spread of tau protein depends on the activation of microglia-this is a key factor that links the influence of amyloid plaque aggregation with the spread of tau protein, and ultimately leads to cognitive impairment and dementia
Pascol said: "Many elderly people have amyloid plaques in their brains, but they never develop Alzheimer's disease
.
" "We know that amyloid accumulation alone is not enough to cause dementia-our findings It shows that it is the interaction between neuroinflammation and amyloid pathology that releases the spread of tau protein, which ultimately leads to widespread brain damage and cognitive impairment
Journal Reference :
Tharick A.
