Your blood stem cells mutate with age, potentially linking your immune system to brain health.

Your blood stem cells mutate with age, potentially linking your immune system to brain health.
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In short: Every day, your body produces billions of new blood cells from bone marrow stem cells. While this process is essential for survival, it is not perfect. As you age, mutated blood stem cells can expand, a phenomenon known as clonal haematopoiesis, which may influence systemic inflammation and even neurodegeneration.

Haematopoiesis is the vital, continuous process of blood cell formation. In healthy adults, this occurs primarily in the bone marrow of the pelvis, cranium, vertebrae, and sternum. Haematopoietic stem cells (HSCs) drive this system through asymmetric division: they self-renew to maintain their own population while simultaneously producing progenitor cells that differentiate into red blood cells, platelets, and various immune cells. This ensures a steady state of blood components, with the body generating between ten billion and one hundred billion new cells daily.

As we age, somatic mutations inevitably accumulate in our tissues. Occasionally, a mutation provides a survival or growth advantage to a stem cell, leading to clonal haematopoiesis (CH). While once considered a niche condition, advanced sequencing reveals that smaller mutant clones are present in most individuals by middle age. By age 70, larger, detectable clones are found in over 10% of the population. These expansions are not merely benign markers of ageing; they can drive systemic inflammation, which is increasingly implicated in the pathogenesis of cardiovascular and autoimmune diseases.

Recent research suggests that this clonal burden may also track with brain health. A study of the Lothian Birth Cohort 1936, involving participants aged 73 to 79, found that clonal haematopoiesis trajectories were significantly associated with cortical atrophy over a six-year period. The observed pattern of brain shrinkage showed spatial similarities to Alzheimer’s disease signatures, particularly in parietal and medial temporal regions. While it remains unclear if CH directly causes Alzheimer’s pathology or simply reflects broader age-related neurodegeneration, these findings position clonal haematopoiesis as a potential candidate marker for adverse brain ageing.

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