Summary: A review examines whether smell loss linked to COVID-19 could raise the risk of dementia later in life.
Source: APS
A recent review of research into how SARS-CoV-2—the virus that causes COVID-19—affects the olfactory system raises important questions about whether COVID-related smell loss might increase the long-term risk of developing dementia.
The review appears ahead of print in the Journal of Neurophysiology (JNP) and synthesizes findings from clinical studies, postmortem analyses, and animal models to explore links between olfactory dysfunction, brain inflammation, and later neurodegeneration.
Loss of smell, or anosmia, was a prominent symptom during the first wave of COVID-19 in 2020. Studies estimated that roughly 77–85% of infected people reported a loss or alteration of smell, often described as parosmia. For most, this deficit resolved relatively quickly, but a substantial subset—estimated at around 15 million people worldwide—continued to experience persistent anosmia or parosmia after recovering from other COVID-19 symptoms. These individuals are sometimes described as “smell long haulers.”
Research indicates that the olfactory sensory epithelium, a region high in the nasal cavity near where olfactory nerve fibers enter the brain’s olfactory bulb, frequently carries a high viral load in people infected with SARS-CoV-2. The olfactory bulb is the brain structure responsible for processing smell and relaying olfactory information to other regions involved in learning, memory, emotion and spatial context.
“The olfactory bulb is involved in much more than detecting odors,” said Leslie M. Kay, Ph.D., the review’s lead author. “It contributes to a sense of place, context, memory, emotion and reward, among other functions.” Because the olfactory sensory epithelium lies so close to the olfactory bulb, inflammation or viral effects in the nose may reach brain structures that support cognition and emotion.
Several lines of evidence support concern about longer-term neurological effects. Clinical data show correlations between olfactory impairment and dementia in conditions such as Alzheimer’s and Parkinson’s disease. Animal studies demonstrate that direct damage to the olfactory bulb can produce anxiety-like and depression-like behaviors. The review highlights findings that SARS-CoV-2 or the immune response it triggers may invade the olfactory bulb, likely through non-neuronal pathways originating in the nasal sensory epithelium, leading to inflammation and early injury to olfactory and limbic brain regions.
Historical parallels also inform current concerns. Prior pandemics have been followed by increased incidence of neurodegenerative conditions in some populations. For example, neurological sequelae observed after the 1918 influenza pandemic included a rise in parkinsonian syndromes among survivors. Population data from Denmark have been interpreted to show that people who had severe influenza had a higher risk of developing Parkinson’s disease roughly a decade later, suggesting that viral infection and inflammation can in some cases initiate or accelerate neurodegenerative processes.
The review argues that COVID-19–related inflammation of the olfactory nerve and damage to the olfactory bulb may set in motion degeneration of connected brain structures and contribute to cognitive and emotional disturbances. While the evidence does not establish a direct causal chain from SARS-CoV-2 infection to dementia, the patterns of early olfactory and limbic dysfunction observed in some patients resemble early-stage changes seen in Alzheimer’s, Parkinson’s and Lewy body dementias.
Currently, few treatments are proven to prevent progressive degeneration following olfactory injury. However, the review suggests that early interventions such as olfactory training and enrichment of sensory and environmental stimulation may offer protective benefits and deserve further study. Because the global COVID-19 pandemic has generated large cohorts of affected individuals and advanced imaging and molecular tools are widely available, researchers now have an unprecedented opportunity to carry out the longitudinal studies needed to clarify long-term outcomes.
“More research is urgently needed—particularly long-term studies that track both smell function and cognitive health in people who have recovered from even mild COVID-19,” Kay said. “Although the pandemic has been a catastrophe in many ways, it also presents a chance to learn more about how viral infection, inflammation and olfactory dysfunction interact with brain aging and neurodegeneration.”
About this COVID-19 and dementia research news
Author: Press Office
Source: APS
Contact: Press Office – APS
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Original Research: Open access.
Title: “COVID-19 and olfactory dysfunction: a looming wave of dementia?” by Leslie M. Kay et al., Journal of Neurophysiology
Abstract
COVID-19 and olfactory dysfunction: a looming wave of dementia?
Olfactory dysfunction is a hallmark symptom of COVID-19 caused by SARS-CoV-2. Sudden anosmia experienced by many patients appears largely peripheral in origin: inflammation and damage to the olfactory sensory epithelium in the upper nasal cavity can prevent odor molecules from activating olfactory sensory neurons.
However, persistent olfactory dysfunction—manifesting as hyposmia (reduced smell) or parosmia (distorted smell)—may affect millions worldwide and represents an ongoing public health concern. Growing evidence indicates that SARS-CoV-2 itself, or inflammation stemming from the immune response in the nasal sensory epithelium, can reach the olfactory bulb, likely via non-neuronal routes. Early injury to the olfactory bulb and connected limbic regions resembles patterns seen in the initial stages of Alzheimer’s, Parkinson’s and Lewy body dementias.
Consequently, long-term olfactory dysfunction accompanied by cognitive or emotional symptoms after COVID-19 could represent the earliest signs of delayed-onset neurodegeneration in some individuals. There is an urgent need for research into effective treatments to prevent degeneration and for longitudinal studies that assess both cognitive and olfactory function in people recovered from COVID-19, including those with only mild initial illness.