Hevin Molecule Shows Promise in Preventing Cognitive Decline in Alzheimer’s Disease
Scientists are exploring various avenues to combat Alzheimer’s and dementia, and a recent study has highlighted the potential of the molecule hevin (or SPARCL-1) in halting cognitive decline.
Hevin is a protein naturally produced in the brain by astrocytes, support cells responsible for maintaining synaptic connections between neurons. Researchers from the Federal University of Rio de Janeiro (UFRJ) and the University of SĂŁo Paulo in Brazil conducted a study where they increased hevin production in the brains of healthy mice and those with Alzheimer’s-like symptoms.
The results were promising: treated mice exhibited enhanced memory and learning abilities compared to untreated mice, with brain scans revealing improved neuron communication at synapses.
Neurobiologist FlĂĄvia Alcantara Gomes from UFRJ explained, “Hevin is a well-known molecule involved in neural plasticity. Our findings demonstrate that overproducing hevin can reverse cognitive deficits in aged animals by enhancing synaptic quality.”
Further analysis revealed that the excess hevin in the mouse brains stimulated the production of other proteins linked to synaptic health, indicating that hevin collaborates with other factors in preserving neuron connectivity.
The study also found lower hevin levels in the brains of Alzheimer’s patients, suggesting a potential role of hevin and astrocytes in the disease. Gomes emphasized, “The novelty lies in understanding the astrocyte’s role in this process, shifting the focus from neurons and highlighting astrocytes as a target for new Alzheimer’s treatment strategies.”
While translating these findings into dementia treatments for humans will take time, the research offers promising prospects to complement existing therapies. Unlike current treatments targeting toxic protein aggregates in the brain, hevin did not influence plaque formation, indicating a more complex pathology for Alzheimer’s.
Biomedical scientist Felipe Cabral-Miranda from UFRJ stated, “The study’s results support the idea that beta-amyloid plaques, while involved in Alzheimer’s mechanisms, may not solely cause the disease.”
Alzheimer’s disease’s complex nature necessitates multifaceted treatment approaches. Gomes mentioned, “Future drug development may replicate hevin’s effects. For now, this research deepens our understanding of Alzheimer’s cellular and molecular mechanisms.”
The study has been published in Aging Cell.
