A new study from Northwell Health found pre-COVID-19 psychotropic medication use is associated with a higher risk for incident dementia following hospitalization for COVID-19 (post-COVID dementia) in older adults.
The study is published in Frontiers in Medicine and was conducted by Yun Freudenberg-Hua et al.
In the study, the team examined the association between pre-COVID psychotropic medication use and one-year incidence of dementia in 1,755 patients hospitalized with COVID-19. The patients were 65 years and older.
The researchers found that the one-year incidence rate of post-COVID dementia was 12.7 percent.
Pre-COVID psychotropic medications and delirium were strongly associated with a higher one-year incidence of post-COVID dementia.
When the analysis was restricted to 423 patients with at least one documented neurological or psychiatric diagnosis at the time of COVID-19 admission, the association between psychotropic medications and incident dementia remained robust.
The greatest associations with post-COVID dementia across different drug classes were seen for antipsychotics and mood stabilizers/anticonvulsants.
The team says this study is no way recommending people should stop taking antipsychotics, but simply that clinicians need to factor in a patient’s medication history while considering post-COVID aftereffects.
Recent studies have found a major cause of fatty liver disease, leaky gut, and COVID-19 vaccine protection is lower and slower in people with liver diseases, which are highly relevant to the current study.
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In a study from the University of Texas, researchers found in a sample of over 400 older adults who had recovered from COVID-19, more than 60% displayed some degree of cognitive impairment.
Problems with thinking were seen even in recovered COVID-19 patients who had only a mild cold or respiratory ailment after virus exposure.
It is not known whether the impairment, such as forgetfulness and language difficulty, will be progressive.
The individuals in the study are over 60 years of age and have been assessed once so far. They will be followed for the next three to five years.
In the study, the team also assessed participants for anosmia, loss of the sense of smell.
The olfactory bulb, which contains the brain cells that react to smell, is primarily where the COVID-19 virus enters the nervous system.
Among the participants, 78% had recovered from SARS-CoV-2 infection that was confirmed by polymerase chain reaction (PCR) testing. Testing confirmed that the other fourth of volunteers were never infected.
Of the 60% of recovered COVID-19 patients who had cognitive impairment, about one in three had severe cognitive impairment.
The team says this could be called “dementia-like syndrome,” because it looks like dementia but may not be persistent or progressive.
People between the ages of 60 and 70 have about a 6% lifetime risk of developing Alzheimer’s disease. The study population reflects a rate of cognitive impairment that is 10 times higher.
Researchers say this could be the start of a dementia-related epidemic fueled by this latest coronavirus.
Another study from Cleveland Clinic found how COVID-19 can lead to Alzheimer’s disease-like dementia.
The findings showed overlap between COVID-19 and brain changes common in Alzheimer’s and may help inform risk management and treatment strategies for COVID-19-associated cognitive impairment.
Reports of neurological complications in COVID-19 patients and “long-hauler” patients whose symptoms persist after the infection clears are becoming more common.
This suggests that SARS-CoV-2 (the virus that causes COVID-19) may have lasting effects on brain function. However, it is not yet well understood how the virus leads to neurological issues.
In that study, the team harnessed artificial intelligence using existing datasets of patients with Alzheimer’s and COVID-19.
They measured the proximity between SARS-CoV-2 host genes/proteins and those associated with several neurological diseases where closer proximity suggests related or shared disease pathways.
The researchers also analyzed the genetic factors that enabled SARS-COV-2 to infect brain tissues and cells.
They found little evidence that the virus targets the brain directly, but they discovered close links between the virus and genes/proteins linked to several neurological diseases, most notably Alzheimer’s, pointing to pathways by which COVID-19 could lead to AD-like dementia.
To explore this further, they examined potential links between COVID-19 and neuroinflammation and brain microvascular injury, which are both hallmarks of Alzheimer’s.
They discovered that SARS-CoV-2 infection strongly altered Alzheimer’s markers implicated in brain inflammation and that certain viral entry factors are highly expressed in cells in the blood-brain barrier.
These findings suggest that the virus may impact several genes or pathways involved in neuroinflammation and brain microvascular injury, which could lead to Alzheimer’s disease-like cognitive impairment.
The researchers also found that individuals with the allele APOE E4/E4, the greatest genetic risk factor for Alzheimer’s, had decreased expression of antiviral defense genes, which could make these patients more susceptible to COVID-19.
Ultimately, the researchers hope to have paved the way for research that leads to testable and measurable biomarkers that can identify patients at the highest risk for neurological complications with COVID-19.
If you care about brain health, please read studies about high blood pressure drugs that could treat vascular dementia and heartburn drugs that could increase risk of dementia.
For more information about brain health, please see recent studies about common liver drug that may treat dementia effectively, and results showing that healthy lifestyle can reduce dementia even if you have a family history of the disease.
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