Cell-Communication Flaw Linked to Higher Alzheimer’s Risk, Danish Study Finds

Cell-Communication Flaw Linked to Higher Alzheimer’s Risk, Danish Study Finds
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Researchers at Aarhus University in Denmark have identified a cellular defect that may help explain how Alzheimer’s disease develops, according to a study reported by ScienceDaily. The team found that a mutation affecting the protein SORLA disrupts the formation of exosomes — tiny particles that enable communication between cells — potentially increasing vulnerability to dementia.

Exosomes are microscopic vesicles released by cells that help regulate activity in surrounding tissue. The new study, published in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association, shows that a mutation in the Sorl1 gene weakens both the quantity and quality of exosomes produced by brain cells. The Sorl1 gene is one of four known to be associated with inherited forms of Alzheimer’s.

Assistant Professor Kristian Juul-Madsen, part of the research team, said cells carrying this mutation produced about 30% fewer exosomes than normal. Moreover, the exosomes that were released were up to 50% less effective at supporting the development and function of nearby cells. The findings suggest exosomes produced by immune cells in the brain play a key role in maintaining neural health. A reduction in healthy exosomes may therefore contribute to the processes that lead to Alzheimer’s disease.

Researchers say the discovery could open new paths for treatment. Potential strategies include enhancing the function of SORLA to restore normal exosome production or targeting other receptors involved in their formation. Alzheimer’s remains the most common form of age-related dementia in Denmark, affecting an estimated 55,000 people, and current treatment options remain limited.