Thread by @ZdenekVrozina

A new review links Alzheimer’s disease, Parkinson’s disease, and COVID-19 through a shared core - neuroinflammation + oxidative stress.
The same pathways, the same immune nodes, the same vulnerabilities of the brain🧵

Key players.
Microglia (the brain’s innate immune cells) and neutrophils (peripheral rapid responders).
When the blood–brain barrier (BBB) is disrupted, neutrophils enter the CNS and inflammation becomes self-amplifying.

Neutrophils can form NETs (neutrophil extracellular traps - DNA + histones + enzymes like MPO/elastase).
In the brain, NETs mean oxidative damage, mitochondrial stress, neuronal injury - and further microglial activation. A vicious cycle.

The authors highlight a central hub - the NLRP3 inflammasome.
ROS, mitochondrial stress, and DAMPs - NLRP3 - IL-1β & IL-18.
They also discuss data showing that Spike S1 can activate microglia/NLRP3 in models, leading to neuroinflammation and cognitive impairment.

CNS damage in COVID is often secondary - systemic inflammation, hypoxia/ischemia, endothelial dysfunction - BBB breakdown - immune cells enter the brain. No heavy viral replication required.

This matters for long COVID. Brain fog doesn’t have to be a vague label - it fits a biological pattern - microglial activation, inflammatory cytokines, redox imbalance. The authors also reference evidence of persistent microglial activity (eg TSPO PET).

One strong point of the paper is the map of shared inflammatory nodes.
TLR2/4, NF-κB, MAPK, NLRP3, IL-1β/IL-6/TNF-α, ROS.
These are not speculative pathways - they are well-established in both neurodegeneration and infection-driven inflammation.

This is a review, not a single large cohort. It integrates animal models, in vitro data, autopsies, clinical observations.

Sum:
COVID-19 can activate the same neuroimmune machinery long implicated in neurodegeneration - chronic inflammation, oxidative stress, vascular dysfunction - mechanisms that can persist once triggered.

By activating shared neuroinflammatory circuits, it may lower the brain’s resilience, accelerate existing vulnerabilities, and leave long-lasting biological footprints. That’s the real warning signal here.

Azul at al., Neuroinflammation and Oxidative Stress in Parkinson’s Disease, Alzheimer’s Disease, and COVID-19: Microglia–Neutrophil Interaction (ACS Omega, 2026). pubs.acs.org/doi/full/10.10…

Nothing groundbreaking - but it’s extremely important that an increasing number of independent groups are systematically putting this together and framing it as a structural, biologically serious warning - while policy continues to ignore ongoing brain injury.
@szupraha @ZdravkoOnline @adamvojtech86 @adamkova_vera

@szupraha Insides.
Signal, not anecdote.
In the Chinese Longitudinal Healthy Longevity Survey (CLHLS), cognitive impairment prevalence increased from 4.3% pre-COVID to 6.8% post-COVID in older adults.
Not a collapse - a population-wide shift toward worse cognitive health.

@szupraha UK Biobank (longitudinal MRI).
After COVID-19, participants showed reduced cortical thickness and global brain volume loss, including people without severe acute disease.
Objective structural changes - not just subjective symptoms.

@szupraha Hospitalized COVID-19 patients (follow-up studies).
Up to 55% showed signs of neurological injury on follow-up, with involvement of olfactory regions and white matter.
Not rare and not subtle.

@szupraha RECOVER-Adult cohort (USA >13,000 participants).
Brain fog and dizziness are among the most common persistent symptoms after infection.
Not a diagnosis - but a population-scale signal.

@szupraha TSPO PET imaging in long COVID.
Increased signal of microglial activation correlates with cognitive and depressive symptoms.
Supports a biological, neuroimmune framework, not a purely psychological one.

@szupraha Post-mortem & multi-omics brain analyses.
Despite low or absent viral RNA, brains show inflammatory signatures, mitochondrial dysfunction, and synaptic/myelin injury, often linked to vascular inflammation.

@szupraha CSF proteomics in COVID-19.
Elevated IL-18, CSF-1, CASP-8 - biomarkers overlapping with early cognitive impairment and neurodegenerative pathways.
Different trigger, familiar biology.