Study reveals new way to slow Alzheimer’s disease progression

Researchers at the Icahn School of Medicine at Mount Sinai in the US have found a new way to slow or even stop the progression of Alzheimer’s disease, which could help develop new treatments for the disease, leading to a step-by-step approach. Memory loss.

The study, published in the journal Nature Neuroscience, provides insight into the role of reactive astrocytes and the “plexin-B1” protein in the pathophysiology of Alzheimer’s disease.

Researchers have found that a type of brain cell that activates in response to injury or disease helps regulate the space around amyloid plaques, affecting how other brain cells approach these harmful deposits. And remove them.

What is Alzheimer’s disease?

Alzheimer’s disease is a progressive neurodegenerative disorder.

Although much research has focused on neurons in the pathogenesis of Alzheimer’s disease, increasing evidence suggests that glial cells, particularly astrocytes, play an important role in the development of the disease.

One of the proteins that has received attention in recent studies is plexin-B1, a receptor known for its role in neuronal development and axon guidance.

Astrocytes are the most abundant glial cells in the central nervous system, and they perform a variety of functions, including maintaining the integrity of the blood-brain barrier, regulating blood flow, and modulating cerebral function.

Reactive astrocytosis

Astrocytes undergo a change called reactive astrocytosis, and this process involves morphological changes, cell proliferation, and secretion of a group of proteins that increase disease severity.

Reactive astrocytes may have protective effects, but they also secrete neurotoxic factors and antioxidants that support neuronal survival, and they contribute to neuroinflammation and nerve cell damage.

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The researchers say that the dual nature of reactive astrocytes makes them a key component in Alzheimer’s disease, and that a protein called plexin-B1 interacts with these cells and affects cytoskeletal dynamics and cellular morphology in the central nervous system.

The new study shows that plexin-B1 signaling affects synaptic plasticity and neuronal survival, and that this protein can be used to modulate the inflammatory response by interacting with different signaling pathways.

Treatment of Alzheimer’s disease

The study’s lead author, Roland Friedel, associate professor of neurology and neurosurgery at Mount Sinai, said the study opens up new avenues for Alzheimer’s disease research, providing a promising path to developing new therapies, focusing on the importance of cell communication in developing treatments for neurodegenerative diseases.

Understanding the role of “plexin-B1” in reactive astrocytes and its contribution to Alzheimer’s disease opens up new horizons for therapeutic interventions, the researchers say, because targeting the signaling of this protein found in astrocytes can alter their reactive state, which can reduce neuroinflammation. and protects neurons from damage.

Although their findings represent a “major advance” in the fight against Alzheimer’s disease, the research team stresses that more research is needed to translate these findings into treatments for human patients.

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