الوضع الليلي
10:0:20 
2023-07-03 
1301
A new study revealed unexpected causes of Alzheimer's disease, in which amyloid plaques were thought to be the main cause of the disease, which gradually leads to memory loss.
Scientists from the University of Pittsburgh School of Medicine, during their study published in the journal "Nature Medicine", concluded that stellate brain cells known as "stellate cells" play an important role in the development of Alzheimer's disease.
The researchers also found, by testing the blood of more than 1,000 elderly people without a cognitive disorder, that those who have a mixture of amyloid and blood markers for activating abnormal astrocytes will develop symptoms of Alzheimer's disease in the future, which is a crucial finding for the development of drugs with a goal of stopping disease progression.
"Our study argues that testing for the presence of brain amyloid along with blood biomarkers of astrocyte interaction is the optimal assay for identifying patients at high risk of developing Alzheimer's disease," said senior author Tharek Pasquale, assistant professor of psychiatry and neuroscience.
"This puts astrocytes at the center as a key regulator of disease progression, challenging the notion that amyloid alone is sufficient to trigger this disease," he continued.
Astrocytes are specialized cells abundant in brain tissue, and just like other members of the glial cells (immune cells in the brain), astrocytes support neurons by supplying them with nutrients and oxygen and protecting them from pathogens.
Alzheimer's disease is a neurodegenerative condition that causes progressive memory loss and dementia, depriving patients of many productive years.
At the tissue level, the hallmark of Alzheimer's disease is the buildup of amyloid plaques - clumps of protein found between nerve cells of the brain - and clumps of disordered protein fibrils, called tangles or tau, that form within nerve cells.
For decades, brain scientists believed that the buildup of amyloid plaques and tangles of tau was not only a sign of Alzheimer's disease but also a proximate cause.
This assumption has also led drug manufacturers to invest heavily in molecules that target amyloid and tau, ignoring the contribution of other brain processes, such as the neuroimmune system.
And recent discoveries by groups like Pascual suggest that disruption of other brain processes, such as increased encephalitis, may be just as important as the burden of amyloid itself in initiating the cascade of neuron death that causes rapid cognitive decline.
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