Zdenek Vrozina Profile picture
Nov 12 15 tweets 3 min read Read on X
A new 5-year study from Brazil shows that surviving COVID-19 can significantly alter the natural course of Alzheimer’s disease (AD).🧵
Patients who had COVID-19 were nearly five times more likely to experience rapid cognitive decline (measured by MMSE).
Their memory, orientation, and mental abilities worsened faster than expected for typical AD progression.
Katz Index scores dropped, showing patients became less able to perform daily activities - washing, dressing, eating.
This decline appeared even after mild COVID-19, not only in those who were hospitalized.
At 5-year follow up, patients who had been hospitalized for COVID-19 showed lower survival than those who never caught the virus.
SARS-CoV-2 can have lasting effects on both health and survival in AD patients.
What it means.
The impact of COVID-19 on AD was detectable years later - not just a temporary post-infection effect.
Cognitive and functional decline occurred across all severities of COVID-19, not only severe cases
The authors suggest that SARS-CoV-2 may accelerate Alzheimer’s pathology, although the precise biological mechanism remains to be determined.
This is the 5-year follow up (!) showing that COVID-19 can accelerate Alzheimer’s progression and worsen long-term outcomes.
People with Alzheimer’s who had COVID-19 may need closer monitoring for faster cognitive and functional decline.
The authors call for larger, multicenter studies to confirm causality and identify risk factors.
Ursi at al., Alzheimer Disease & Associated Disorders 2025. Alzheimer Disease Patients Who Survived COVID-19 Have Rapid Disease Progression and a Higher Risk of Death at 5-year Follow-up. journals.lww.com/alzheimerjourn…
Previous work already hinted at this:
Wang et al., 2022 (J. Alzheimer’s Disease) - COVID-19 increased the risk of a new Alzheimer’s diagnosis by 50-80 % in older adults.
BMC Geriatrics, 2024 - meta analysis confirmed higher risk of new-onset dementia after COVID-19. Etc.
Ursi et al., 2025 now adds the missing piece - in those already living with AD, SARS-CoV-2 can speed up the disease itself.
These findings highlight a growing blind spot in pandemic policy.
Faster cognitive decline after COVID-19 means more patients entering advanced Alzheimer’s stages sooner -increasing the burden on families, caregivers, and already overstretched healthcare systems.
Yet, there are no systematic post-COVID monitoring or prevention programs for neurodegenerative outcomes.
Ignoring this link between infection and brain aging is a public health failure in slow motion. @szupraha @ZdravkoOnline @adamvojtech86
@szupraha @ZdravkoOnline @adamvojtech86 To clarify - the two earlier studies (Wang et al., 2022; BMC Geriatrics 2024) looked at new-onset dementia or Alzheimer’s disease after COVID-19 in people who had no prior diagnosis.
They showed that infection can trigger or accelerate the appearance of Alzheimer-like pathology.
@szupraha @ZdravkoOnline @adamvojtech86 By contrast, this Ursi 2025 focused on patients who already had Alzheimer’s disease before infection.
It shows that COVID-19 can accelerate the existing neurodegenerative process itself - leading to faster cognitive decline, loss of independence, and higher mortality.
@szupraha @ZdravkoOnline @adamvojtech86 Together, these findings outline a double impact
the possibility of more new Alzheimer’s cases emerging after COVID-19
faster progression in those already affected
Both trends increase the long-term burden on healthcare systems and caregivers.

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More from @ZdenekVrozina

Nov 10
A interesting paper in Nature Structural & Molecular Biology finally reveals how metformin really works inside mitochondria.
It doesn’t shut down energy - it fine-tunes the flow of electrons through complex I🧵
Complex I is the engine of the respiratory chain.
It transfers electrons from NADH to coenzyme Q10 (ubiquinone) and pumps protons across the membrane to make ATP - the cell’s energy currency.
For years, it was believed that metformin simply blocks this engine.
But a full block would be toxic - cells would lose energy.
The new study shows a smart mechanism - metformin acts only when the enzyme is open and active.
Read 15 tweets
Nov 8
What if SARS-CoV-2 doesn’t just infect - but also self-assembles into molecular structures that keep the immune system burning?
Zhang showed that after the virus breaks apart, some of its fragments re-form peptide-RNA nanocrystals that potently activate TLR3, even without live virus - a “viral afterlife.”🧵
Let’s start with what we actually know.
Zhang showed that some of SARS protein fragments can self-assemble with RNA into nanocrystalline structures that strongly activate the immune receptor TLR3 - even without live virus
The authors call this phenomenon a “viral afterlife.”
Read 25 tweets
Nov 7
Long COVID in women and men are not the same disease. They share symptoms, but diverge in biology - immune, hormonal, and genetic.
After months since the preprint -
peer-reviewed study is now out in Cell Reports Medicine.🧵
This is the complete analysis immunity, hormones, and gene expression in 78 Long COVID with ME-CFS patients.
It confirms what patients have said for years -
this condition is biological, measurable, and deeply sex-specific.
In women, the immune system never stands down.
chronic inflammation, exhausted T cells, and loss of regulatory Tregs
leaky gut - constant immune activation
high IL-6, IL-1α, TNF-α, IFN-γ
low testosterone and cortisol - hormones that normally keep inflammation in check.
It’s not overreaction. It’s immune dysregulation.
Chronic inflammation meets hormonal collapse.
Read 19 tweets
Nov 7
Getting the COVID and flu shot together?
A new Italian study in Cytokine found that the early inflammatory response after getting COVID-19 and flu vaccines at the same time may actually limit how long your antibody protection lasts🧵
29 healthcare workers received both
an mRNA COVID-19 (XBB.1.5) booster
a quadrivalent inactivated flu shot.
Blood was collected
before vaccination (T0)
5 days later (T1)
after 3 months (T2)
after 6 months (T3)
Within just 5 days, levels of inflammatory cytokines shot up -
especially IL-6, CXCL10, and TNF-α.
In some people, IL-8 also spiked and strongly correlated with IL-6.
That means their innate immune system went into high gear.
Read 10 tweets
Nov 7
A new study from Hong Kong Baptist University examined how mRNA COVID-19 vaccines might influence insulin signaling.
The finding?
The spike protein can interfere with metabolic pathways - but mainly in people with type 2 diabetes (T2D)🧵
In mice given 4 doses of the mRNA vaccine, researchers observed impaired glucose tolerance, reduced insulin sensitivity, and higher triglycerides.
At the molecular level, phosphorylation of IRβ and Akt - key insulin signaling steps - was reduced.
Liver transcriptomics showed activation of NF-κB, MAPK, and AMPK-related pathways.
Read 11 tweets
Nov 5
A new study in The Lancet Child & Adolescent Health followed nearly 14 million children in England.
It shows that SARS-CoV-2 infection leaves long-term marks on the vascular and immune system - even in kids.
Not just for weeks, but measurable up to a year later🧵
After COVID-19, children had a sharply increased risk of
systemic inflammatory syndromes (MIS-C, etc)
venous thrombosis
thrombocytopenia
myocarditis and pericarditis
And part of these risks remained elevated 12 months post-infection.
That means - even if a child feels fine after COVID, the body may stay in a dysregulated immune and vascular state - with lingering inflammation and endothelial stress.
In biological terms, COVID leaves a footprint
Read 13 tweets

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