Alzheimers Dementia: What are the differences in hematologic neurodegenerative markers between hospitalized COVID-19 patients and uninfected patients?

Neurological complications, particularly encephalopathy, are common among hospitalized COVID-19 patients, and nearly 50 percent of hospital survivors persist with long-term cognitive abnormalities

In hospitalized COVID-19 patients with emerging clinical evidence of cognitive impairment, particularly toxic metabolic encephalopathy [TME], biomarkers of neuronal and glial damage in the blood are elevated and neurodegeneration Elevated biomarkers of sex were associated with a higher risk of in-hospital death and a lower rate of discharge home

Neurofilament light chain (NfL), a cytoskeletal intermediate filament protein that integrates with axons in the central and peripheral nervous systems, has been noted to be elevated in COVID-19 patients, as well as glial fibrillary acidity protein (GFAP), which is a specific indicator of glial/astrocyte damage, and ubiquitin carboxy-terminal hydrolase L1 (UCHL1) and total tau (t-tau), a neuron-specific protein

Phosphorylated tau-181 (p-tau181) and amyloid beta (Aβ) 40 and 42, which are more specific biomarkers of AD-type pathology

Notably, UCHL1, GFAP, tau, and NfL are also elevated after disruption of the blood-brain barrier (BBB), which has been documented in neuropathological studies and AD in COVID-19 deceased patients

With this, Jennifer A.

Ubiquitin carboxy-terminal hydrolase L1 (UCHL1) and amyloid beta (Aβ40,42) between the presence or absence of encephalopathy, in-hospital death and survival, discharge home and other treatments

They found that t-tau, p-tau181, GFAP, and NfL were significantly elevated in patients with encephalopathy and in-hospital deaths on admission, whereas t-tau, GFAP, and NfL were significantly lower in those discharged home

COVID patients had higher NfL, GFAP and UCHL1 than non-COVID controls with MCI or AD