Overview: Research questions whether loss of smell associated with COVID-19 infection may increase the risk of developing dementia later in life.
A review of studies examining the effect of SARS-CoV-2 – the virus that causes COVID-19 – on the olfactory system raises questions about whether loss of smell associated with COVID-19 infection increases the risk of developing dementia later in life. can increase life.
The review will be published in the 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 loss or alteration of smell (parosmia).
While most people recover quickly from this dysfunction, an estimated 15 million people around the world are considered to have “smelling breath” after otherwise recovering from COVID-19. They experience persistent anosmia or parosmia.
Studies have shown that the olfactory epithelium, which is located in the upper part 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 parts of the brain for processing. These other brain areas are involved in learning, memory, and emotion.
“All this means that the [olfactory bulb] is involved in much more than just smelling. It is involved in sense of place, memory, context, emotion, reward, and many other processes,” said Leslie M. Kay, 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. An association has also been found between a disturbed sense of smell and dementia in some people with neurodegenerative disorders such as Alzheimer’s and Parkinson’s disease. Animal studies have shown that damage to the lamp leads to anxiety and a depression-like state.
“Previous pandemics also support the theory that “viral invasion of the [central nervous system] can be a trigger for neurodegeneration, resulting in a later neurological deficit,” explains Kay. The 1918 Spanish flu pandemic led to a surge in people developing Parkinson’s disease, and data from Denmark shows that people who have had the flu have a 70% higher risk of developing Parkinson’s disease ten years later.
“The review provides evidence suggesting that inflammation in the olfactory nerve and damage to the olfactory bulb via COVID-19 infection and immune response may also cause degeneration of brain structures related to the olfactory system and cognitive impairment.
More research is needed and is possible thanks to the technological advances available to scientists during the current pandemic,” Kay said.
“While the COVID-19 pandemic is a catastrophe on many levels, it offers an opportunity to improve human health.”
About this COVID-19 and dementia research news
Author: press office
Contact: Press agency – APS
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Original research: Open access.
“COVID-19 and olfactory dysfunction: an impending wave of dementia?” by Leslie M. Kay et al. Journal of Neurophysiology
COVID-19 and olfactory dysfunction: an impending wave of dementia?
Olfactory dysfunction is a hallmark symptom of COVID-19 disease due to the SARS-CoV-2 virus.
The cause of the sudden and usually temporary anosmia that most people suffer from COVID-19 is likely completely peripheral – inflammation and other damage caused by the virus in the sensory epithelium in the upper recesses of the nasal cavity can damage chemicals or prevent them from being released. are properly activated the olfactory sensory neurons.
However, persistent olfactory dysfunction from COVID-19, in the form of hyposmia and parosmia (reduced or altered smell), can affect as many as 15 million people worldwide.
Thus, this epidemic of olfactory dysfunction is an ongoing public health concern. Mounting evidence suggests that the SARS-CoV-2 virus itself or an inflammation from the immune response in the nasal sensory epithelium can enter the olfactory bulb, probably through non-neuronal transmission. COVID-19-related long-term olfactory dysfunction and early damage to olfactory and limbic brain regions suggests a pattern of degeneration similar to that seen in early stages of Alzheimer’s, Parkinson’s and Lewy Body dementia.
For example, long-term olfactory dysfunction in combination with cognitive and emotional impairment from COVID-19 may be the first signs of delayed onset of dementia due to neurodegeneration.
Few treatments are known to be effective in preventing further degeneration, but the first line of defense against degeneration can be olfactory and environmental enrichment.
There is an urgent need for more research into treatments for olfactory dysfunction and longitudinal studies, including cognitive and olfactory function of patients who have recovered from even mild COVID-19.