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Can a Brain‑Produced Molecule Unlock Cognitive Recovery in Dementia?

Marco Aurélio Gomes Veado

3 min read

June 9, 2025

In Brazil, researchers from the Federal University of Rio de Janeiro (UFRJ) and collaborators from the University of São Paulo (USP) have discovered that a molecule called hevin can reverse cognitive impairment.

The study, conducted in mice, showed that this glycoprotein produced by brain cells (astrocytes) is able to increase the connections between neurons (synapses) in aged rodents and in animal models of Alzheimer’s disease.

Image generated by AI (Freepik)

What is Hevina, and Why Astrocytes Matter

Astrocytes are star-shaped glial cells that support neurons. They secrete hevina—a molecule critical for neural plasticity. The team increased hevina production in the brains of aged mice and genetically modified mice resembling Alzheimer’s disease. The result? Improved synaptic connectivity, more, stronger connections between neurons—and measurable improvements in memory and learning.

Professor Flávia Alcantara Gomes (UFRJ) explains: “Hevina is well known and involved in neural plasticity... we found that overproduction can reverse cognitive deficits in aged animals by improving synaptic quality”

The Evidence is Promising

The study, published in Aging Cell, included proteomic analysis of the rodents’ brains. They observed 89 proteins with altered expression linked to enhanced synaptic function. Despite cognitive gains, the beta‑amyloid plaque burden in the hippocampus remained unchanged.

This adds momentum to theories that beta‑amyloid is not the sole driver of Alzheimer’s disease, prompting a shift toward alternative targets like astrocytes.

Why This Matters to MCI and Beyond

At MCI and Beyond, we focus on early intervention, neuroplasticity, and holistic approaches to Memory Care. This study aligns perfectly: it underscores the potential of astrocyte-based therapies and biomolecules like hevina in reversing mild cognitive impairment and dementia.

Key implications for our community:

  1. New therapeutic targets beyond beta‑amyloid.
  2. Reinforces the concept of engaging brain plasticity even in later stages.
  3. Highlights the relevance of glial cells, long overlooked in dementia research.

Challenges Ahead: From Molecule to Medicine

While the results are exciting, bridging the gap from mice to humans will require overcoming major hurdles:

  • Blood–brain barrier: Scientists must engineer hevina‑like compounds that cross this barrier effectively.
  • Safety and efficacy: Rigorous testing is needed to ensure translation into human treatments.
  • Complex disease mechanics: Alzheimer’s is multifactorial; a single-target therapy may not address all symptoms.

As the lead researcher states, “We still have a long way to go before this molecule becomes a drug, but the fundamental gain is understanding cellular and molecular mechanisms in Alzheimer’s and aging”.

What’s Next for Research and Care

  • Preclinical development: Optimizing hevina analogues to cross the brain barrier.
  • Human trials: Eventually, phase I trials to evaluate safety in humans.
  • Integrative therapy models: Combining strengthened glial support with lifestyle changes, cognitive training, and existing therapeutics.

Conclusion

The discovery of hevina’s role in reversing cognitive decline marks a promising stride toward neurorestorative therapies. It shifts focus from neuron-only models to include glial‑driven neuroplasticity, a paradigm in line with our holistic approach at MCI and Beyond.

While more research is needed, this breakthrough offers hope and direction for future dementia treatments. We'll continue monitoring developments as they move from bench to bedside.

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