Summary: Research questions whether loss of smell associated with COVID-19 infection increases the risk of dementia later in life.
A source: APS
A review of studies on the effects of the virus that causes SARS-CoV-2-COVID-19 on the olfactory system raises questions about whether the loss of smell associated with COVID-19 infection may increase the risk of developing dementia later in life.
The review will be published before the publication Journal of Neurophysiology (JNP).
Loss of smell (anosmia) is one of the specific symptoms associated with the first wave of COVID-19 in 2020, with an estimated 77-85% of people infected with the virus having a loss or change in smell (parosmia).
Although most people recover quickly from this dysfunction, an estimated 15 million people worldwide are considered “odor long carriers” after recovering from COVID-19. They suffer from persistent anosmia or parosmia.
Studies have shown that the olfactory epithelium—located in the upper part of the nose, near where the olfactory nerve enters the olfactory bulb in the brain—carries a higher viral load in people infected with SARS-CoV-2.
The olfactory bulb is a structure in the brain that controls the sense of smell and sends sensory information to other areas of the brain for processing. These other brain regions deal with learning, memory and emotion.
“That’s what it all means [olfactory bulb] It involves more than just smell. It is involved in place, memory, context, emotion, reward, and many other processes,” said review author Leslie M. Kay, Ph.D.
Because the olfactory epithelium is located close to the olfactory bulb, it is possible that COVID-19 infection may affect cognitive function even after recovery. A link between impaired sense of smell and dementia has also been found in some people with neurodegenerative conditions such as Alzheimer’s and Parkinson’s disease. Animal studies have shown that damage to the bulb causes anxiety and depression-like conditions.
“Previous pandemics also” support the viral invasion theory [central nervous system] can trigger neurodegeneration, which later leads to neurological deficits,” Kay explained. The 1918 Spanish flu pandemic led to a wave of people developing Parkinson’s disease, and data from Denmark showed that people who had the flu had a 70% risk of developing Parkinson’s ten years later. increases to
“The trial offers evidence that inflammation of the olfactory nerve and damage to the olfactory bulb through COVID-19 infection and the immune response, as well as damage to brain structures associated with the olfactory system, can lead to cognitive impairment.
More research is needed and possible because of the technological advances available to scientists during the current pandemic,” Kay said.
“Although a catastrophe on many levels, the COVID-19 pandemic offers an opportunity to improve human health.”
This is about COVID-19 and dementia research news
Author: Press service
A source: APS
The connection: Press service – APS
Photo: Image is in the public domain
Original research: Open access.
“Covid-19 and olfactory dysfunction: a coming wave of dementia?” Leslie M. Kay et al. Journal of Neurophysiology
COVID-19 and olfactory dysfunction: a coming wave of dementia?
Olfactory dysfunction is a hallmark of the SARS-CoV-2 virus, COVID-19.
The cause of the sudden and usually temporary anosmia that most people experience with COVID-19 may be entirely peripheral—viral-induced inflammation and other damage to the sensory epithelium inside the upper nasal cavities can impair the proper activation of chemicals. olfactory neurons.
However, permanent impairment of olfactory function in the form of hyposmia and parosmia (reduced or altered sense of smell) from COVID-19 may affect up to 15 million people worldwide.
Thus, this epidemic of olfactory dysfunction is an ongoing public health concern. Additional evidence suggests that the SARS-CoV-2 virus itself or an inflammatory immune response in the nasal sensory epithelium may enter the olfactory bulb, likely through non-neuronal transmission. The long-term impairment of olfactory function associated with COVID-19 and the early damage to olfactory and limbic brain regions suggest a pattern of degradation seen in the early stages of Alzheimer’s, Parkinson’s, and Lewy Body dementia.
Thus, long-term olfactory dysfunction and cognitive and emotional impairments caused by COVID-19 may be delayed early signs of neurodegenerative dementia.
Several treatments are known to be effective in preventing further deterioration, but the first line of defense against deterioration may be olfactory and environmental enrichment.
Treatment of olfactory dysfunction and longitudinal studies, including more research on cognitive and olfactory function in patients who have recovered from mild COVID-19, are needed.