Vipin M. Vashishtha Profile picture
Jan 31 12 tweets 4 min read Read on X
Researchers found a link between COVID-19 & blood markers linked to faulty proteins in the brain. They found people who had previously had COVID-19 were more likely to have increased levels of biomarkers linked to faulty amyloid proteins—a hallmark for Alzheimer's disease. 1/ Image
On average, the effects were comparable to 4 years of aging with the greatest effects seen in those hospitalized with severe COVID-19 or with underlying risk factors for dementia such as smoking or high blood pressure. 2/ Image
The findings suggest that mild or moderate COVID may accelerate biological processes that contribute to buildup of disease-promoting amyloid in brain. This raises possibility that COVID-19 might contribute to an increase in later risks of developing Alzheimer's disease. 3/ Image
These findings suggest COVID-19 may drive changes which contribute to neurodegenerative disease. This may be due to the inflammation triggered by the disease, although how this inflammation might impact the brain and changes to amyloid is not yet fully clear. 4/ Image
However, the researchers can’t say that catching the SARS-CoV-2 virus directly causes these changes, or if it does, by how much a single episode of infection increases someone's risk. 5/
But these findings do suggest that COVID-19 may increase the risk of Alzheimer's in the future—as has been suggested in the past for other kinds of infections—especially among people with pre-existing risk factors. 6/ Image
Amyloid is a common protein with a range of functions in the body. But the buildup of an abnormal form of the protein, called beta amyloid (Aβ), is a key component of many diseases. 7/ Image
Aβ forms the characteristic clumps seen in the brains of patients with Alzheimer's disease, which are thought to cause damage to the neurons in the brain, leading to changes in cognition and behavior. 8/ Image
In this study, the researchers found SARS-CoV-2 infection was associated w/ changes in several blood proteins previously linked to brain Aβ pathology. The magnitude of changes was similar to that associated w/ a well-known genetic risk factor for AD, a genetic variant: APOE4 9/ Image
Greater changes found in older participants & those hospitalized with COVID-19-19 or had a history of hypertension. These correlated with poorer cognitive test scores & measures of overall health as well as changes in brain imaging patterns associated w/neurodegeneration 10/ Image
More studies now are needed to prove any causal links. Ultimately, the more we know about factors that contribute to dementia risk—whether they are directly under our control, like lifestyle or diet, or modifiable by vaccines or early treatment for infectious diseases. 11/11 Image
Here is the link to the study👇

nature.com/articles/s4159…

• • •

Missing some Tweet in this thread? You can try to force a refresh
 

Keep Current with Vipin M. Vashishtha

Vipin M. Vashishtha Profile picture

Stay in touch and get notified when new unrolls are available from this author!

Read all threads

This Thread may be Removed Anytime!

PDF

Twitter may remove this content at anytime! Save it as PDF for later use!

Try unrolling a thread yourself!

how to unroll video
  1. Follow @ThreadReaderApp to mention us!

  2. From a Twitter thread mention us with a keyword "unroll"
@threadreaderapp unroll

Practice here first or read more on our help page!

More from @vipintukur

Dec 20
A new review highlights how neurotropic viruses like SARS-CoV-2 reprogram the metabolism of brain immune cells — especially microglia and astrocytes — contributing to neuroinflammation and brain dysfunction.

➡️ Under normal conditions, glial cells use oxidative phosphorylation (OXPHOS) to support brain homeostasis and anti-inflammatory functions. But viral infection shifts them toward aerobic glycolysis, driving pro-inflammatory cytokine production and immune activation. 1/Image
This metabolic switch:

• increases inflammatory mediators (IL-1β, TNF-α)
• elevates oxidative stress
• impairs neuronal support
• disrupts the blood-brain barrier

All of which can exacerbate neuroinflammation and damage. 2/ Image
For SARS-CoV-2 specifically, the viral S1 protein can cross the BBB and trigger microglial activation and inflammasome (NLRP3) signaling, which further promotes inflammation and potentially persistent neurological effects. 3/ Image
Read 5 tweets
Dec 16
Breakthrough in respiratory virus prevention (Flu, COVID & more)

➡️ Researchers have developed an AI-designed intranasal antiviral platform that could block multiple respiratory viruses—flu, COVID-19, and future variants—right at the entry point: the nose. 1/ Image
The platform is based on interferon-lambda, a natural antiviral protein, redesigned using AI protein engineering to overcome major limitations: poor heat stability and rapid clearance from nasal mucosa.

➡️ Using AI, scientists strengthened unstable protein regions, improved solubility, and added glycoengineering—making the protein so robust it remained stable for 2 weeks at 50 °C. 2/Image
To keep it in the nose longer, the protein was packaged in nanoliposomes and coated with chitosan, greatly improving adhesion to nasal mucosa and penetration through thick mucus. 3/ Image
Read 5 tweets
Dec 15
New study in International Journal of Infectious Diseases highlights persistent immune alterations after SARS-CoV-2 infection—providing further biological evidence for #LongCOVID as a genuine post-infectious condition.

➡️ Researchers found lasting changes in immune activation and regulation, even months after recovery from acute COVID-19—suggesting the immune system does not fully reset after infection. 1/Image
Key findings point to chronic inflammation, altered cytokine responses, and immune imbalance, which may explain prolonged symptoms such as fatigue, pain, and neurocognitive complaints.

➡️ Importantly, these immune changes were seen independent of initial disease severity, reinforcing that even mild COVID-19 can have long-term immunological consequences. 2/Image
Image
The study of >40,000 people shows that key immune cells (T cells, B cells, NK cells) dropped during widespread COVID infection and stayed below pre-pandemic levels for nearly 2 years. 3/ Image
Read 4 tweets
Dec 13
A new Israeli study demonstrates why some people develop #LongCOVID.

➡️ By analysing immune responses, gene expression and plasma proteins in blood samples, scientists found that people with longCOVID show persistent chronic inflammation and disrupted immune signalling months after infection — patterns not seen in those who fully recovered. 1/Image
These immune differences help explain lingering symptoms — such as fatigue, brain fog and breathlessness — and point to specific inflammatory pathways that could be targeted for treatment. This work opens new avenues for better therapies for millions living with longCOVID. 2/ Image
Researchers performed immunological, virological, transcriptomic and proteomic analyses from a cohort of 142 individuals between 2020 and 2021, including uninfected controls (n = 35), acutely infected individuals (n = 54), convalescent controls (n = 24) and patients with LC (n = 28).

➡️ The LC group was characterized by persistent immune activation and proinflammatory responses for more than 180 days after initial infection compared with convalescent controls, including upregulation of JAK-STAT, interleukin-6, complement, metabolism and T cell exhaustion pathways.

➡️ Similar findings were observed in a second cohort enrolled between 2023 and 2024, including convalescent controls (n = 20) and patients with LC (n = 18). 3/Image
Read 4 tweets
Dec 3
Can past COVID-19 weaken the body’s ability to fight tuberculosis?

➡️ A new study comparing immune responses to SARS-CoV-2 and Mycobacterium tuberculosis (MTB) suggests COVID-19 may dampen both antiviral and anti-TB immunity — even months later. 1/ Image
Researchers tested immune cells from healthy individuals and COVID-19 survivors, both with and without latent TB infection (LTBI).

➡️ They stimulated the cells with SARS-CoV-2 Spike and MTB antigens and measured cytokine responses. 2/ Image
Key finding:

➡️ People who recovered from COVID-19 showed significantly reduced inflammatory cytokines — IFN-γ, IL-2, IL-6, TNF-α — in response to both SARS-CoV-2 and MTB antigens.

➡️ Suggests prolonged immune downregulation after COVID-19. 3/ Image
Read 5 tweets
Dec 1
A new study comparing immune profiles months after COVID-19 vs influenza shows that SARS-CoV-2 leaves behind distinct and longer-lasting immune abnormalities — very different from what is seen after flu. 1/ Image
Post-COVID patients showed increased CXCR3 and CCR6 expression across multiple lymphocyte populations.

➡️ Punjabi This means their immune system is still sending signals for cells to migrate into tissues (especially the lungs) months after infection.

➡️ Persistent tissue-homing = prolonged inflammation. 2/Image
In contrast, post-flu patients mainly showed a decrease in CCR4 on naïve T cells, monocytes, and dendritic cells — a very different and less persistent pattern.

➡️ Flu does not drive the same long-term immune activation. 3/ Image
Read 5 tweets

Did Thread Reader help you today?

Support us! We are indie developers!


This site is made by just two indie developers on a laptop doing marketing, support and development! Read more about the story.

Become a Premium Member ($3/month or $30/year) and get exclusive features!

Become Premium

Don't want to be a Premium member but still want to support us?

Make a small donation by buying us coffee ($5) or help with server cost ($10)

Donate via Paypal

Or Donate anonymously using crypto!

Ethereum

0xfe58350B80634f60Fa6Dc149a72b4DFbc17D341E copy

Bitcoin

3ATGMxNzCUFzxpMCHL5sWSt4DVtS8UqXpi copy

Thank you for your support!

Follow Us!

:(