Can We Slow Brain Aging? Research Explores “Rejuvenation” Proteins in Dementia
Aging is the biggest risk factor for dementia, but what if we could tap into biological mechanisms that slow down brain aging? A growing body of research suggests that factors circulating in our blood may influence the brain’s resilience to neurodegenerative diseases. Scientists have lonsg observed that when older mice receive young blood, their cognitive abilities improve, while young mice exposed to aged blood show signs of accelerated brain aging. These findings hint at the presence of ‘pro-aging’ and ‘pro-youthful’ factors in the bloodstream that could shape brain health.
A new study led by Casaletto et al., including Adam Boxer of UCSF, takes this concept one step further by investigating these rejuvenation factors in humans. Their research focused on cerebrospinal fluid (CSF)—the liquid surrounding the brain and spinal cord—to see whether proteins associated with brain aging in animal models might have similar effects in people with dementia.
The study examined five key proteins: C-C motif chemokine ligand 11 (CCL11), C-C motif chemokine ligand 2 (CCL2), beta-2-microglobulin (B2M), osteocalcin (BGLAP), and colony stimulating factor 2 (CSF2, also known as granulocyte-macrophage colony-stimulating factor or GM-CSF). Higher levels of these proteins—particularly CSF2 and BGLAP—were associated with better cognitive function, slower disease progression, and lower levels of neurodegeneration markers in people with Alzheimer’s disease and genetic forms of frontotemporal dementia (FTD). In other words, these ‘pro-youthful’ proteins may help protect the brain from the effects of aging and disease.
One of these factors, CSF2 (GM-CSF) has received particular attention at the University of Colorado, Anschutz Medical Campus, as part of a clinical trial in Alzheimer’s disease. CSF2 plays a key role in immune system function, stimulating the production of certain white blood cells. A recent clinical trial testing GM-CSF in Alzheimer’s disease patients found encouraging results, including improved cognitive scores and changes in Alzheimer’s-related biomarkers. This suggests that boosting CSF2 levels might have therapeutic potential.
While this research is still in its early stages, it highlights a fascinating new direction in dementia treatment. Instead of focusing solely on disease-specific pathology, targeting the broader aging process itself could open new doors for prevention and therapy. The next steps will involve larger studies and clinical trials to determine whether these rejuvenation proteins can be leveraged to slow or even prevent neurodegeneration in aging individuals. The dream of a ‘youthful’ brain, even in later life, may not be as far-fetched as it once seemed.
Reference: Casaletto KG, Saloner R, Kornak J… Pressman PS… Boxer A, Brain aging rejuvenation factors in adults with genetic and sporadic neurodegenerative disease, Brain Commun. 2025 Jan 15;7(1):fcae432. doi: 10.1093/braincomms/fcae432
Written with assistance from Claude AI by Anthropic.