COVID-19 Tied to Acceleration of Alzheime... - Cure Parkinson's

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COVID-19 Tied to Acceleration of Alzheimer's Pathology, Parkinson's as well?

sharoncrayn profile image
4 Replies

A very interesting and well done study out of NYU. While focusing on ALZ, it obviously has ramifications across all neurodegenerative diseases, such as PD. In many respects this answers the question that many PwP had regarding infection from Covid-19 or its variants.

COVID-19 Infection Associated with Uptick in Alzheimer’s Biomarkers in the Blood

Certain biological markers in blood — including total tau (t-tau), neurofilament light (NfL), glial fibrillary acid protein (GFAP), ubiquitin carboxyl-terminal hydrolase L1 (UCH-L1), and species of amyloid beta (Aβ40, Aβ42) and phosphorylated tau (pTau-181) — are indicators of injury in the brain, neuroinflammation and Alzheimer’s disease.

To study the presence of these blood biomarkers, neurodegeneration and neuroinflammation in older patients who were hospitalized with COVID-19, Thomas Wisniewski, M.D., a professor of neurology, pathology and psychiatry at New York University Grossman School of Medicine, and colleagues took plasma samples from 310 patients who were admitted to New York University Langone Health with COVID-19. Of the patients, 158 were positive for SARS-CoV-2 with neurological symptoms and 152 were positive for SARS-CoV-2 without neurologic symptoms. The most common neurological symptom was confusion due to toxic-metabolic encephalopathy (TME).

In patients who were initially cognitively normal with and without TME related to COVID-19 infection, the researchers found higher levels of t-tau, NfL, GFAP, pTau-181, and UCH-L1 in COVID-19 patients with TME compared to COVID-19 patients without TME. There were no significant differences with Aβ1-40, but the pTau/Aβ42 ratio showed significant differences in patients with TME. Additionally, t-tau, NfL, UCH-L1 and GFAP significantly correlated with markers of inflammation such as C-reactive peptide, which may suggest inflammation-related blood-brain barrier disruption accompanying neuronal/glial injury.

“These findings suggest that patients who had COVID-19 may have an acceleration of Alzheimer’s-related symptoms and pathology,” Wisniewski said. “However, more longitudinal research is needed to study how these biomarkers impact cognition in individuals who had COVID-19 in the long term.”

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sharoncrayn
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asmckay profile image
asmckay

Hi Sharon. Thank-you for this. Your last post, on the Pfizer and the delta variant, disappeared. Did you change your mind on anything that you said in that article? Thanks

sharoncrayn profile image
sharoncrayn in reply to asmckay

No, I did not change my mind. It was deleted as were the posts between MBA and myself. However, the new study out of the Mayo Clinic absolutely confirms my original supposition. Why the significant decline in effectiveness from DELTA occurred with Pfizer I have no idea. Sample size was huge (25,000). Troubling.

Comparison of two highly-effective mRNA vaccines for COVID-19

during periods of Alpha and Delta variant prevalence

asmckay profile image
asmckay in reply to sharoncrayn

Thanks Sharon. I didn't see the posts between MBA and you. I opened your post within 5 mins of you posting it and read it much later. I think that it is a shame that it was deleted. Much better for objections to be visible.

sharoncrayn profile image
sharoncrayn in reply to asmckay

Agreed. The PHE study was in the public domain.

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