A review of studies on the effect of SARS-CoV-2 – the virus that causes COVID-19 – on the olfactory system raises questions about whether the loss of smell associated with COVID-19 infection might increase the risk of dementia later in life.
The review was published prior to printing at Journal of Neurophysiology (JNP).
Loss of smell (anosmia) is one of the hallmark symptoms associated with the first wave of COVID-19 in 2020, with an estimated 77-85% of people infected with the virus reporting a loss or alteration of their sense of smell (parosmia).
Although most people recover quickly from this dysfunction, an estimated 15 million people worldwide are considered “long-distance odor fanatics” after recovering from COVID-19. They suffer from persistent loss of smell or parosmia.
Studies have shown that the olfactory sensory epithelium – located in the upper area of the nose, near where the olfactory nerve enters the olfactory bulb in the brain – carries a high viral load in people infected with SARS-CoV-2.
The olfactory bulb is the structure in the brain that manages the sense of smell and sends sensory information to other areas of the brain for processing. These other brain regions are involved in learning, memory, and emotion.
“All of this means that [olfactory bulb] It is involved in much more than smell. It is involved in a sense of place, memory, context, emotion, reward, and many other processes, said Leslie M.K., Ph.D., author of the review.
Due to the proximity of the olfactory sensory epithelium to the olfactory bulb, COVID-19 infection can affect cognitive function even after recovery. A relationship has also been found between a disrupted sense of smell and dementia in some people with neurodegenerative conditions such as Alzheimer’s disease and Parkinson’s disease. Animal studies have shown that damage to the onion results in anxiety and depression.
Previous epidemics also support the theory that ‘viral invasion of [central nervous system] It can be a trigger for neurodegeneration leading to subsequent neurological deficits,” explained Kay. The 1918 Spanish Flu pandemic led to a wave of people developing Parkinson’s disease, and data from Denmark found that people who had the flu had a 70% risk of developing Parkinson’s disease after a decade.
The review provides evidence that inflammation to the olfactory nerve, damage to the olfactory bulb by COVID-19 infection, and the immune response may also cause degeneration of brain structures associated with the olfactory system and cognitive impairment.
“More research is needed and is possible because of the technological advances available to scientists during the current pandemic,” Kay said.
“While a disaster on many levels, the COVID-19 pandemic presents an opportunity to improve human health.”
About this COVID-19 and dementia research news
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Contact: Press Office – APS
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original search: open access.
“Covid-19 and the sense of smell: A looming wave of dementia?” by Leslie M. Kay et al. Journal of Neurophysiology
COVID-19 and the sense of smell: A looming wave of dementia?
An impaired sense of smell is a hallmark symptom of COVID-19 caused by the SARS-CoV-2 virus.
The cause of the sudden, usually temporary loss of smell that most people experience with COVID-19 is likely entirely peripheral – inflammation and other virus-induced damage to the sensory epithelium within the upper nasal cavity can damage the chemicals or prevent them from properly activating cells Olfactory sensory neuron.
However, persistent olfactory dysfunction caused by COVID-19, in the form of hyposmia and parsomia (reduced or altered smell) may affect up to 15 million people worldwide.
Thus the epidemic of olfactory dysfunction is an ongoing public health concern. Increasing evidence suggests that SARS-CoV-2 itself or inflammation induced by an immune response in the nasal sensory epithelium may invade the olfactory bulb, most likely by non-neuronal transmission. COVID-19 associated with long-term olfactory dysfunction and early damage to the olfactory and limbic brain regions indicates a pattern of degeneration similar to that seen in the early stages of Alzheimer’s disease, Parkinson’s disease and Lewy body dementia.
Thus, long-term olfactory dysfunction combined with cognitive and emotional distress from COVID-19 may be the first signs of delayed onset of dementia from neurodegeneration.
Few treatments are known to be effective to prevent further deterioration, but the first line of defense against degeneration may be olfactory and environmental enrichment.
There is an urgent need for more research on treatments for olfactory impairment and longitudinal studies including cognitive and olfactory function from patients who have recovered from even mild COVID-19.