Your sense of smell gives you a superpower. Without moving a muscle or opening your eyes, it helps you detect danger, store or trigger memories, discern flavors, or get a rush of feel-good chemicals during a meal. You can imagine that losing your sense of smell (a problem doctors call anosmia [aˈnäzmēə]) can be devastating. Millions of people experienced it as a side effect of COVID-19. Other conditions also can lead to anosmia. 

Medical experts are also finding that a change in or diminishing sense of smell can be an early warning about several diseases. So, pay particular attention to any diminishing abilities since your sense of smell and memory are handled in the same areas of the brain. 

According to the NIH Institute on Aging and Harvard Research, the loss of smell (anosmia) is a well-established early warning sign of dementia, especially Alzheimer’s disease, and can appear many years before noticeable memory loss. 

At Yale School of Medicine, neuroscience research has theorized that Parkinson’s Disease originates in the part of the brain that controls the sense of smell. Approximately 75 percent to 90 percent of people with Parkinson’s Disease report a diminished sense of smell up to 10 years before their diagnosis. 

The sense of smell is processed in the olfactory system, which is connected to brain regions critical for memory and cognition, such as the frontal and temporal lobes. Damage to these areas — often caused by Alzheimer’s-related pathology — can impair both smell and memory. In Alzheimer’s, harmful proteins like amyloid-beta and tau accumulate in olfactory and memory-related brain regions before spreading elsewhere. 

Longitudinal brain imaging found that older adults with better smell scores had slower loss of brain volume in frontal and temporal areas, and slower decline in memory, attention, and processing speed. 

PET scan studies showed that lower olfactory test scores were linked to higher levels of Alzheimer’s biomarkers, especially in regions tied to both smell and memory. 

APOE ε4 gene carriers (who have a higher Alzheimer’s risk) began losing smell sensitivity a decade earlier than non-carriers, and this decline was associated with faster cognitive decline. 

Rapid smell loss over time predicted structural brain changes and higher dementia risk, even before cognitive symptoms appeared. 

Smell decline can be an early biomarker for Alzheimer’s and other dementias. It may help identify people at risk before memory problems become obvious, enabling earlier intervention or enrollment in clinical trials. However, smell loss can also occur from other causes (e.g., sinus disease, nasal injury), so it should be interpreted alongside other assessments. 

A reduced sense of smell should be taken very seriously. It is not just a minor sensory change — it can be a silent signal of early brain changes in dementia or Parkinson’s. Monitoring smell function may one day be part of routine screening for early detection and prevention strategies.  

One hopeful note is that the olfactory system is one of the most plastic sensory systems in the brain, meaning it can adapt and change in response to experience, environmental cues, and internal state. The system’s lifelong ability to generate new neurons, makes it uniquely adaptable and the possibility of generating new neurons in the same area of the brain where memory resides may offer an eventual path to slow the progress of dementia or Parkinson’s Disease.