The scientific world is yet to understand the full extent to which smells can unravel the secrets of the mind and brain. Notably, many researchers have studied whether scents might help revive lost memories in people suffering from conditions such as dementia, Alzheimer’s, and other forms of memory loss. Some studies show promise, but there are still no large-scale, definitive clinical trials. Nevertheless, a few hospitals and senior care facilities have begun offering kiosks of nostalgic scents designed to evoke cherished memories.
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Interestingly, smell loss has now emerged as an early detectable sign of Alzheimer’s, which damages and destroys cells in the brain over time. The neurodegenerative disease is both the most common and most devastating form of dementia due to its prevalence, progression, and lack of cure.
The buildup of beta-amyloid (Aβ) plaques outside brain cells and the clumping of tau proteins into tangles are key signs of Alzheimer’s disease. There is still no cure, but new antibody treatments that target Aβ can slightly slow cognitive decline in people with early-stage Alzheimer’s. However, these treatments work best when the disease is detected as early as possible.
In a recent study published in Nature Communications, researchers have shown that Alzheimer’s disease often starts with non-memory symptoms—one of the earliest being a reduced sense of smell. However, scientists don’t yet fully understand why this happens. In Alzheimer’s, damage begins early in a small brain region called the locus coeruleus (LC), which produces the chemical noradrenaline—important for processing smells. In mice with early-stage Alzheimer’s, the nerve fibers carrying signals from the LC to the brain’s smell centre (the olfactory bulb) were lost before any amyloid plaques appeared.
The researchers discovered that immune cells in the olfactory bulb (called microglia) were mistakenly destroying these LC nerve fibres. The researchers found clear evidence of altered membrane composition in the affected nerve fibres. They observed that phosphatidylserine—a fatty substance that protects nerve cells in the brain and enables them to communicate with each other—shifted its position. Ideally, it should have been located on the inner side of a neuron’s membrane, but it got shifted to the outer surface.
When this whole process was blocked, both the nerve fibres and the animals’ sense of smell were preserved. Similar signs of damage were also found in human patients in the early Alzheimer’s stage.
The study authors suggest that early smell loss in Alzheimer’s may be caused by damage to noradrenaline pathways—and that testing a person’s sense of smell, along with brain imaging, could help diagnose the disease much earlier.
