Researchers have unveiled an unexpected connection between clonal hematopoiesis of indeterminate potential (CHIP) and a reduced susceptibility to developing Alzheimer’s disease (AD). CHIP, characterized by the expansion of mutated blood cells, is typically associated with a higher risk of various diseases, including leukemia and cardiovascular problems. However, this study has revealed that individuals with CHIP may have a lower likelihood of developing AD, providing new insights into the role that blood cells play in brain health.
Alzheimer’s disease, a devastating condition with no cure, has long been a focus of scientific investigation. A recent study uncovered a remarkable connection between a condition called clonal hematopoiesis of indeterminate potential (CHIP) and a reduced risk of developing Alzheimer’s. CHIP is known for altering the DNA of certain blood cells and increasing the risk of blood cancers and cardiovascular disease. This unexpected finding could offer insights into the role of blood cells in brain health.
The Intriguing World of Blood Cells
Blood Cell Renewal: Blood cells have relatively short lifespans and must be continuously replenished. Hematopoiesis, the process of producing new blood cells, primarily takes place in the bone marrow. Hematopoietic stem cells (HSCs) in the bone marrow multiply to replace depleted blood cells, typically resulting in exact copies. However, in CHIP, some hematopoietic stem cells undergo genetic changes, leading to the production of slightly different blood cells.
CHIP and Health Risks: People with CHIP can live for many years but face an increased risk of blood cancer and cardiovascular disease compared to those without CHIP. This condition is particularly common among older adults, with an estimated 10% to 30% of individuals over 70 years old having CHIP. While most research on CHIP has focused on its impact on cardiovascular health, its influence on the brain has remained a largely unexplored territory.
Unveiling the Alzheimer’s Connection
To bridge this knowledge gap, a research team led by Stanford University scientists delved into how CHIP may affect the risk of developing Alzheimer’s in older adults. They embarked on a study that involved analyzing blood samples from 1,362 individuals with Alzheimer’s and 4,368 without the disease. By sequencing the DNA from blood cells, the researchers identified who had CHIP. Astonishingly, their findings revealed that people with CHIP had a significantly reduced risk of developing Alzheimer’s.
In the next phase of their study, the team sequenced the DNA of microglia in the brains of eight individuals with CHIP. Microglia are the brain’s immune cells, crucial for brain function and health. In Alzheimer’s, microglia often fail in their protective role, damaging the neurons they should safeguard. Interestingly, the researchers found that seven of these individuals had microglia in their brains that carried the same CHIP variant found in their blood cells. Although not definitive, this observation hints that certain variant blood cells might migrate to the brain, potentially supporting microglial function.
Overall, these findings suggest that CHIP may offer a level of protection against Alzheimer’s disease. Future research will delve into the differences between brain immune cells carrying CHIP variants and those that do not. Understanding why CHIP is associated with reduced Alzheimer’s risk could hold the key to slowing the progression of this debilitating disease.
This study has unveiled a remarkable link between CHIP and a reduced risk of developing AD. While further research is needed to fully understand the mechanisms at play, this unexpected finding could revolutionize our understanding of Alzheimer’s and offer potential insights into the role of blood cells in brain health.
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Haider M. Hassan, Data Scientist, Bridge Informatics
Haider is one of our premier data scientists. He provides bioinformatic services to clients, including high throughput sequencing, data pre-processing, analysis, and custom pipeline development. Drawing on his rich experience with a variety of high-throughput sequencing technologies, Haider analyzes transcriptional (spatial and single-cell), epigenetic, and genetic landscapes.
Before joining Bridge Informatics, Haider was a Postdoctoral Associate at the London Regional Cancer Centre in Ontario, Canada. During his postdoc, he investigated the epigenetics of late-onset liver cancer using murine and human models. Haider holds a Ph.D. in biochemistry from Western University, where he studied the molecular mechanisms behind oncogenesis. Haider still lives in Ontario and enjoys spending his spare time visiting local parks. If you’re interested in reaching out, please email [email protected] or [email protected]