Novel Molecule Demonstrates Potential to Reverse Age-Related Cognitive Decline in Animal Studies

Researchers from Brazil have identified a promising molecule named Hevin that may counteract cognitive deficits associated with aging and dementia. Conducted through experiments with mice, the study revealed that Hevin, a glycoprotein produced by astrocytes—support cells in the brain—can enhance neuronal connections, or synapses, in aged animals and models of Alzheimer's disease.

The study, published in the journal Aging Cell, shows that increasing Hevin levels in the brain improved cognitive functions without affecting the accumulation of amyloid plaques, which are traditionally linked to Alzheimer's disease. Despite the common focus on these plaques, the findings suggest that cognitive decline and neural deterioration can be alleviated independently of plaque reduction.

Dr. Flávia Alcantara Gomes, leading the Cellular Neurobiology Laboratory at UFRJ, explained that Hevin plays a crucial role in neural plasticity—how the brain adapts and rewires itself. The research demonstrated that overproduction of Hevin can restore synaptic health and improve learning and memory in aged mice.

While these findings offer hope for new pathways in treating neurodegenerative diseases, the study is still at an early stage, primarily in animal models. Future research will need to address whether Hevin or similar compounds can cross the blood-brain barrier and become effective drugs for humans. Nonetheless, this work underscores the importance of astrocytes in neurodegenerative disease processes and opens avenues for therapeutic strategies targeting glial cells.

The team used advanced proteomic analysis to understand how Hevin influences brain proteins involved in synaptic function, revealing changes that promote stronger neuron-to-neuron communication. Interestingly, overexpression of Hevin did not alter the typical hallmarks of Alzheimer's, like amyloid deposits, highlighting the multifactorial nature of the disease and the potential of targeting different mechanisms.

According to Dr. Felipe Cabral-Miranda, the findings support a broader view that amyloid plaques may not be the sole cause of Alzheimer's symptoms, suggesting alternative therapeutic targets focused on cellular support systems like astrocytes.

This study adds significant knowledge to the field, emphasizing the importance of glial cells in brain health and offering a promising target for future drug development to combat cognitive decline.

Source: [https://medicalxpress.com/news/2025-05-molecule-reverses-cognitive-deficits-aging.html]