Natural molecule reverses age- and dementia-related cognitive decline. In a new study, researchers identified a molecule produced by a particular type of brain cell that reversed the cognitive decline seen in both healthy aging and dementia. It provides a deeper understanding of the aging process and a potential target for future treatments.
In a new study, researchers identified a molecule produced by a particular type of brain cell that reversed the cognitive decline seen in both healthy aging and dementia. It provides a deeper understanding of the aging process and a potential target for future treatments.
“Hevin is a well-known molecule involved in neural plasticity,” said the study’s co-corresponding author, Flávia Alcantara Gomes, PhD, head of the Cellular Neurobiology Laboratory in the Institute of Biomedical Sciences at UFRJ. “It’s naturally secreted by cells in the central nervous system that support the functioning of neurons and are known as astrocytes. We found that the overproduction of hevin is capable of reversing cognitive deficits in aged animals by improving the quality of synapses in these rodents.”
Astrocytes are large cells that actively support and protect nerve cells (neurons), including the connections, or synapses, between them. They are involved in the formation, function, and elimination of synapses, the regulation of brain chemistry, and even influence synaptic plasticity, the brain’s ability to adapt and change over time. Astrocytes secrete hevin, a type of protein that helps regulate how synapses form and function by influencing how neurons interact with one another.
The researchers started by examining public health data and found that hevin levels were decreased in the brains of people with Alzheimer’s disease compared to healthy people of the same age. Moving on to mice, they found that hevin was also decreased in mouse models of Alzheimer’s disease. This led the researchers to consider whether manipulating the levels of hevin in astrocytes would affect the signs and symptoms of Alzheimer’s disease.
After causing the overproduction of hevin in some mice and not in others, the researchers found that boosting hevin levels prevented cognitive decline in both the Alzheimer’s mouse models and the healthy middle-aged mice. Interestingly, though, the researchers observed that elevated hevin levels didn’t have any effect on beta-amyloid plaques, the buildup of which is a hallmark of Alzheimer’s disease.
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