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Olfactory dysfunction or partial loss of smell is one of the earliest symptoms of Alzheimer’s disease (AD). While accumulation of the toxic amyloid β protein in the brain is known to drive AD progression, its involvement with olfactory sensory neurons is poorly understood. Researchers have now dug deeper into the molecular mechanisms underlying olfactory dysfunction by assessing behavioral, physiological, and anatomical changes in a mouse model of AD. These findings could help reveal therapeutic targets for AD.
Loss of smell or olfactory dysfunction is an early indication of the neurodegenerative Alzheimer’s disease (AD) and appears in approximately 90% of all patients. While loss of smell is a major symptom, patients with AD are only unable to recognize specific odors and do not completely lose their sense of smell; this suggests a possible region-specific involvement of the olfactive center in the brain. Amyloid β (Aβ), a toxic protein that accumulates in t