Amyloid processing in COVID-19-associated neurological syndromes

Area of Science:

• Neuroscience
• Immunology
• Infectious Diseases

Background:

• SARS-CoV-2 infection can cause neurological damage with various manifestations.
• Mechanisms underlying COVID-19 neurological injury remain poorly understood.

Purpose of the Study:

• To investigate biomarkers of amyloid processing, neuronal injury, astrocyte activation, and neuroinflammation in patients with COVID-19 neurological syndromes.
• To explore the relationship between these biomarkers and neurological manifestations.

Main Methods:

• Cross-sectional exploratory prospective biomarker cohort study.
• Compared 21 patients with COVID-19 neurological syndromes to 23 healthy controls.
• Measured cerebrospinal fluid (CSF) and serum biomarkers including amyloid precursor proteins, neurofilament light (NfL), glial fibrillary acidic protein (GFAp), and cytokines (TNF-ɑ, IL-6, IL-1β, IL-8).

Main Results:

• Patients with COVID-19 neurological syndromes showed significantly reduced CSF soluble amyloid precursor protein-ɑ (sAPPɑ) and sAPPβ, and amyloid-beta (Aβ) 40, Aβ42, and Aβ42/Aβ40 ratio compared to controls.
• Significantly increased NfL and pro-inflammatory cytokines were observed in patients, negatively correlating with sAPPɑ and sAPPβ.
• GFAp was significantly reduced in patients, positively correlating with sAPPɑ and sAPPβ.

Conclusions:

• This pilot study suggests impaired amyloid processing in patients with COVID-19 neurological syndromes.
• Altered amyloid processing is linked to increased neuronal injury and neuroinflammation, but reduced astrocyte activation.