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Brain Amyloid + Abnormal Astrocyte Activation Together Can Predict Hidden Alzheimer’s Risk Better, Says New Study

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Breakthrough Discovery: Blood Test Predicts Hidden Alzheimer’s Risk in Cognitively Healthy Elderly

Can Your Blood Really Help Predict Hidden Alzheimer’s Risk? Yes, according to new findings.

Why do certain individuals develop Alzheimer’s disease while others do not? Moreover, why do many individuals with abundant toxic amyloid aggregates in their brains, a characteristic feature of Alzheimer’s pathology, never experience Alzheimer’s-associated dementia? A groundbreaking study published in Nature Medicine by researchers from the University of Pittsburgh School of Medicine appears to have unraveled the answer.

The research highlights that astrocytes, a type of star-shaped brain cells, play a crucial role in determining the progression of Alzheimer’s disease. Through an extensive analysis involving over 1,000 elderly individuals with and without amyloid pathology but without cognitive impairment, the team led by the University of Pittsburgh discovered that only those who exhibited a combination of amyloid burden and blood markers indicating abnormal activation or reactivity of astrocytes were likely to develop symptomatic Alzheimer’s in the future. This significant breakthrough offers invaluable insights for the development of drugs aimed at impeding disease progression.

This new study “argues that testing for the presence of brain amyloid along with blood biomarkers of astrocyte reactivity is the optimal screening to identify patients who are most at risk for progressing to Alzheimer’s disease,” adds senior author Tharick Pascoal. “This puts astrocytes at the center as key regulators of disease progression, challenging the notion that amyloid is enough to trigger Alzheimer’s disease.”

Alzheimer’s disease is a progressive neurodegenerative disorder characterized by the gradual loss of memory and dementia, depriving individuals of many productive years. At the tissue level, the defining feature of Alzheimer’s disease is the accumulation of amyloid plaques—clumps of protein aggregates lodged between brain nerve cells—as well as the formation of tau tangles, which are disordered protein fibers found inside neurons.

For a long time, neuroscientists believed that the buildup of amyloid plaques and tau tangles not only signaled the presence of Alzheimer’s disease but also directly caused it. This belief resulted in substantial investments by pharmaceutical companies in developing drugs targeting amyloid and tau, while overlooking the potential contribution of other brain processes, such as the neuroimmune system.

However, recent findings by researchers like Pascoal suggest that the disruption of other brain processes, such as heightened brain inflammation, may be equally crucial to the initiation of the pathological cascade leading to neuronal death and rapid cognitive decline, alongside the burden of amyloid.

In his earlier studies, Pascoal and his team discovered that brain tissue inflammation triggers the propagation of abnormally folded proteins in the brain, directly contributing to cognitive impairment in individuals with Alzheimer’s disease.

Now, nearly two years later, researchers have unveiled a blood test that can predict cognitive impairment.

Astrocytes, which are highly abundant in the brain tissue, are specialized cells. Similar to other glial cells, which are immune cells residing in the brain, astrocytes fulfill essential functions in supporting neuronal cells. They provide nutrients and oxygen to neurons, as well as safeguard them against pathogens. Initially, due to their lack of electrical conduction and apparent absence in direct neuronal communication, the significance of glial cells, including astrocytes, in maintaining health and their involvement in diseases had been disregarded. However, recent studies conducted at Pitt have revolutionized this understanding.

“Astrocytes coordinate brain amyloid and tau relationship like a conductor directing the orchestra,” adds lead author Bruna Bellaver. “This can be a game-changer to the field, since glial biomarkers in general are not considered in any main disease model.”

Blood samples from elderly individuals without cognitive impairment were analyzed by scientists in three separate studies to identify biomarkers related to astrocyte reactivity. The presence of glial fibrillary acidic protein (GFAP) and pathological tau were examined. The results revealed that individuals who tested positive for both amyloid and astrocyte reactivity exhibited signs of progressive tau pathology, indicating a predisposition to developing clinical symptoms of Alzheimer’s disease.

These findings carry significant implications for future clinical trials involving potential Alzheimer’s drugs. To intervene in disease progression at earlier stages, trials are increasingly targeting pre-symptomatic individuals. Therefore, accurate early diagnosis of Alzheimer’s risk becomes crucial for successful trials. It is important to note that a substantial portion of amyloid-positive individuals will not develop clinical Alzheimer’s. Thus, amyloid positivity alone is insufficient to determine eligibility for therapy.

To enhance patient selection for later stages of Alzheimer’s, it is recommended to include astrocyte reactivity markers like GFAP in the diagnostic test panel. This approach enables improved identification of patients more likely to progress to advanced Alzheimer’s stages. Consequently, it aids in refining the selection of candidates for therapeutic interventions who are more likely to benefit from them.

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