Growing new brain cells may help some people resist Alzheimer’s disease
Why does one person develop severe Alzheimer’s while another with equally damaged brain tissue stays sharp into their eighties?
The question of whether adult humans produce new neurons at all has been fiercely debated for years. In mice, the evidence is clear: a brain region called the hippocampus — central to memory and spatial navigation, and among the first areas affected by Alzheimer’s — generates new nerve cells throughout life. In humans, the picture has been far murkier, partly because the human brain is vastly harder to study than a rodent’s, and partly because the biological details appear to differ significantly between species.
Recent research adds an important piece to this puzzle. Scientists examined brain tissue from deceased individuals, some of whom had Alzheimer’s disease and some of whom had not shown cognitive decline — despite carrying similar burdens of the protein deposits, beta-amyloid plaques and tau tangles, that are hallmarks of the condition. People who had remained cognitively intact showed significantly more signs of active neurogenesis — the birth of new nerve cells — in their hippocampus than those who had experienced cognitive decline.
Resilience, not just damage
This represents a meaningful shift in how Alzheimer’s is being conceptualised. For decades, research focused primarily on beta-amyloid accumulation as the central driver of the disease, generating the hypothesis that clearing these plaques should halt its progression. That theory has now consumed billions of dollars in failed clinical trials. The emerging perspective asks a different question: not only what goes wrong, but why some brains appear far more capable of withstanding the same damage.
Adult hippocampal neurogenesis could be one such protective mechanism. New neurons may partially compensate for damaged neural circuits, modulate inflammatory processes in brain tissue and maintain the flexibility of memory networks. If so, the presence of Alzheimer’s proteins is not automatically equivalent to Alzheimer’s disease — the outcome may depend substantially on how well the brain can regenerate itself alongside the accumulating damage.
Can neurogenesis be boosted?
Animal studies suggest that physical exercise, cognitive stimulation and certain dietary patterns can increase hippocampal neurogenesis. Whether the same holds true in humans, and to what degree, remains insufficiently established. There is also methodological friction: critics have pointed out that many studies on human neurogenesis may be measuring technical artefacts — distortions introduced by the measurement process itself rather than actual biological activity.
The field sits in an intriguing but unresolved position. The hypothesis that individual variation in neurogenesis partly determines who develops Alzheimer’s and who does not is biologically plausible and increasingly supported by evidence. But the tools to prove it conclusively in living humans do not yet exist — which means the most important question remains open.