Breakthrough Discovery: Brain Cells Linked to Reduced Dementia Risk Unveiled

In a groundbreaking study, scientists have pinpointed two distinct types of brain cells associated with a reduced risk of dementia, even among individuals who display the brain abnormalities typically associated with Alzheimer’s disease. The results of this research, published in the journal Cell on September 28, may offer new avenues for safeguarding these protective cells and ultimately preventing cognitive decline in aging populations.

Related article: Gut Microbiome Composition Offers Insights for Diagnosis and Intervention of Early Alzheimer’s Disease

Bridging the Gap between Brain Abnormalities and Cognitive Impairment

The prevailing theory surrounding Alzheimer’s disease implicates the accumulation of sticky amyloid proteins in the brain as the root cause. These proteins lead to the formation of amyloid plaques, which gradually destroy neurons and, consequently, memory and cognitive function. 

However, not all individuals experiencing cognitive impairment in late life exhibit amyloid clumps, and not everyone with amyloid buildup develops Alzheimer’s. To address this puzzling disparity, a team of researchers, including neurobiologist Hansruedi Mathys from the University of Pittsburgh School of Medicine and neuroscientist Li-Huei Tsai from the Massachusetts Institute of Technology (MIT), embarked on a comprehensive investigation.

Discovering Resilient Cells Guarding Against Cognitive Decline

The research team examined brain tissue samples from 427 deceased participants who had undergone cognitive and motor skill assessments throughout their lives. The samples were taken from the prefrontal cortex, a region integral to higher cognitive functions. Using gene sequencing, the scientists identified two critical cell types characterized by specific genetic markers: one with active genes responsible for reelin, a protein normally involved in neuronal migration in the developing brain through control of cell–cell interactions, linked to brain disorders such as schizophrenia, and the other with active genes encoding somatostatin, a hormone regulating various bodily processes.

The groundbreaking discovery revealed that individuals with greater cognitive impairment had lower quantities of these protective cells, whereas those with no cognitive deficits displayed higher counts of these cells, even when they exhibited significant amyloid deposits—an indicator of Alzheimer’s disease. Intriguingly, these protective cell types identified by the researchers were inhibitory neurons, responsible for halting neuronal communication. This revelation opens up new possibilities for understanding cognitive functions affected during Alzheimer’s.

A Paradigm Shift in Alzheimer’s Research

While most Alzheimer’s research has historically centered on excitatory neurons, responsible for transmitting electrical signals to activate other neurons, this study underscores the significance of inhibitory cells. These cells, armed with reelin or somatostatin, might play an undiscovered role in preserving cognitive function amidst Alzheimer’s disease. It is hypothesized that inhibitory cells with these markers are especially vulnerable in Alzheimer’s patients, shedding light on why some individuals with significant amyloid buildup do not display symptoms.

This groundbreaking discovery is being hailed as a significant step forward in Alzheimer’s research. Traditional efforts have largely focused on combating amyloid plaques within the brain. However, this latest breakthrough offers new prospects for protecting vulnerable brain cells instead. The research’s innovative single-cell sequencing technique and the resulting atlas of protective cells have been deemed “state of the art” by experts in the field, providing an invaluable starting point for future studies as sequencing technology advances. The quest to combat Alzheimer’s has taken a promising turn, emphasizing the importance of understanding and preserving specific cell types as potential keys to unlocking effective treatments and prevention strategies.

Author

Sinead Huang