A Promising New Target: Hevin and Cognitive Health in the Rio Study
A recent study from researchers in Rio de Janiero highlights a fascinating shift in Alzheimer’s research—beyond neurons and amyloid plaques, into the vital role of glial support cells. They found that increasing levels of Hevin (also known as SPARCL‑1) in hippocampal astrocytes can reverse cognitive decline in mice with both normal aging and Alzheimer’s-like pathology.
What the Rio Study Did
Hevin levels are lower in human Alzheimer’s brain tissue and in mouse models Using an adeno‑associated virus vector, they forced astrocytes to overexpress Hevin in the hippocampus of middle‑aged wild‑type and Alzheimer’s‑model mice
After 1–6 months, treated mice performed significantly better in tests like novel object recognition and spatial navigation—even though amyloid plaque levels remained unchanged
Why This Matters
Cognitive improvements occurred independent of plaque clearance, casting doubt on amyloid-centric theories and highlighting synaptic strengthening via astrocytic functions
Proteomic analyses showed Hevin-enhanced synaptic proteins, meaning better synapse formation and signaling
My Conclusion:
The Rio study highlights a different path to cognitive resilience—through astrocytes, not plaques. For APOE4 carriers, this adds hope: leveraging synaptic support and glial health may be a powerful counterbalance to genetic risk.
While there is no supplement to directly impact hevin levels, there are things we can do to support Hevin expression.
🔬 Natural and Lifestyle Strategies (based on mechanistic overlap):
1. Exercise
Aerobic exercise boosts astrocytic support, BDNF, and anti-inflammatory glial signaling.
While Hevin itself wasn’t directly measured, mouse studies show increased synaptogenic factors in active brains.
Voluntary wheel running in rodents increased astrocytic gene expression related to synapse formation.
2. Omega-3 Fatty Acids (DHA)
DHA enhances astrocyte health and synaptic function.
DHA increases the expression of synaptogenic genes and reduces APOE4-mediated synapse loss, similar to Hevin.
May synergize with Hevin pathways, though not shown to increase Hevin directly.
3. Astrocyte-supportive compounds
While no direct data on Hevin exists, these support the cells that produce it:
Lithium (low dose) – promotes glial differentiation, synaptogenesis, and neuroplasticity.
Butyrate (e.g., tributyrin) – promotes anti-inflammatory astrocyte phenotypes via HDAC inhibition.
Resveratrol – activates SIRT1, supports synaptic plasticity, and reduces glial inflammation.
Sodium phenylbutyrate – not natural, but used in research to boost astrocyte-related synaptogenic genes.
4. Sleep optimization
Hevin is regulated by circadian cues and sleep deprivation decreases key astrocytic proteins.
Prioritizing deep sleep may help maintain Hevin expression.
5. Red/Near-Infrared Light Therapy (PBM)
PBM supports astrocyte mitochondrial health, improves synaptic repair, and activates glial-derived neurotrophic support.
Though Hevin hasn’t been directly measured in PBM studies, its role in synapse formation makes it a logical downstream beneficiary.