Vipin M. Vashishtha Profile picture
Jan 31, 2025 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…

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More from @vipintukur

Jan 24
Post-COVID fatigue isn’t just subjective.
Using advanced MRI, researchers found real changes in brain blood flow and oxygen metabolism in people with Post-COVID-19 Syndrome (PCS) after mild infection.

➡️ Key finding:

PCS patients showed increased oxygen metabolism in the hippocampus (memory hub) but reduced metabolism in the anterior cingulate cortex (ACC) — despite no visible brain atrophy. 1/Image
Why this matters:

➡️ Higher hippocampal metabolism was linked to better cognitive performance, suggesting a compensatory response to maintain thinking and memory in PCS. 2/ Image
In contrast, lower anterior cingulate cortex (ACC) metabolism correlated with:

• depressive symptoms
• reduced motivation
• higher inflammatory & glial markers (TNF-α, GFAP)
➡️ pointing to immune-driven neurovascular uncoupling. 3/ Image
Image
Read 4 tweets
Jan 22
Why do some people feel exhausted long after COVID-19?

➡️ New brain-imaging research shows that even after mild COVID, people with persistent fatigue can have subtle but real changes in brain structure.

➡️ These changes are not large or widespread, but tend to appear in connected brain networks, especially areas involved in attention, decision-making, and sensory processing. 1/Image
Image
Importantly, the brain regions affected overlap with areas that naturally express TMPRSS2, a protein that helps SARS-CoV-2 enter cells — suggesting certain brain circuits may be more vulnerable to the virus. 2/ Image
The study also links these changes to brain chemical systems involved in mood, energy, and cognition (serotonin, acetylcholine, glutamate, and cannabinoids). 3/ Image
Read 4 tweets
Jan 19
COVID-19 doesn’t just affect the lungs — it can disrupt how cells produce energy. New research shows that COVID-19 alters the genetic “switches” that control mitochondria, the structures that power our cells. 1/ Image
By comparing people who died from severe COVID-19, those who recovered, and healthy individuals, researchers found lasting changes in how mitochondrial genes are regulated. These changes were most prominent in genes involved in energy production and metabolism. 2/ Image
Importantly, people with COVID-19 showed abnormally high levels of proteins that control mitochondrial structure and stress responses, suggesting long-term damage to the cell’s energy system. 3/ Image
Read 5 tweets
Dec 26, 2025
#LongCOVID (LC) shares striking symptom overlap with hypermobility spectrum disorders (HSD/hEDS): fatigue, brain fog, dysautonomia, pain—especially in women.

➡️ A new case series explores whether some “intractable” LC may reflect undiagnosed hypermobility disorders.

➡️ Five women with persistent LC symptoms were evaluated at an hEDS/HSD clinic.
All met Beighton score criteria for hypermobility.

➡️ 4 diagnosed with hEDS, 1 with HSD
➡️ 3 had dysautonomia

None had prior hypermobility diagnoses. 1/Image
All patients carried MTHFR polymorphisms (C677T or A1298C)—recently linked to hEDS/HSD.

➡️ Several also showed features of mast cell activation, suggesting immune dysregulation may unmask latent connective tissue disorders after SARS-CoV-2 infection.

➡️ Targeted management (physical therapy, methylfolate/B12, mast cell stabilization, pain interventions) led to clinical improvement in all cases.

🔑 Takeaway: Consider hEDS/HSD in women with refractory Long COVID, especially with multisystem pain and dysautonomia. 2/Image
This case series suggests that some patients with severe, persistent #LongCOVID—especially women—may have previously undiagnosed hypermobility disorders (hEDS/HSD).

➡️ Five women with refractory LongCOVID symptoms were found to meet criteria for hypermobility, often with dysautonomia, mast cell–related features, and MTHFR polymorphisms.

➡️ Targeted management led to clinical improvement, highlighting the need to consider hEDS/HSD in patients with intractable Long COVID symptoms. 3/
Read 4 tweets
Dec 26, 2025
🔥 A landmark study challenges the long-held belief that Alzheimer’s disease (AD) is irreversible.

➡️ Using advanced mouse models that mimic human AD pathology, researchers found that restoring and maintaining healthy levels of NAD⁺, a key cellular energy molecule, can not only prevent but also reverse advanced Alzheimer’s pathology and fully restore cognitive function in mice. 1/Image
The team showed that NAD⁺ deficiency is a central driver of AD pathology—leading to blood-brain barrier breakdown, neuroinflammation, oxidative damage, and impaired neurogenesis. 2/ Image
➡️ By administering a compound that rebalances NAD⁺ (P7C3-A20), all these pathological features were reversed, and memory and cognitive function were recovered.

➡️ These effects were seen in both amyloid-driven and tau-driven models, with supporting evidence from human AD brain samples suggesting disrupted NAD⁺ homeostasis in patients. 3/Image
Image
Read 5 tweets
Dec 24, 2025
As we age, our immune system becomes less effective, partly because key cells called CD8⁺ T-cells have trouble forming long-lasting memory.

A new study shows that a process called autophagy — the cell’s way of cleaning out old or damaged components — plays a central role in this problem. 1/Image
When a T-cell divides, it can make two daughter cells with different future roles: one becomes a long-lived ‘memory T cell’ that helps protect against future infections, and the other becomes a short-lived ‘effector T cell’ that fights the immediate infection.
For this to happen, the cell must sort its internal parts unevenly during division. 2/Image
The researchers found that #autophagy helps clear out old mitochondria before division, allowing daughter cells to inherit different mitochondrial content.

➡️ This asymmetric inheritance is crucial for creating a mix of T-cells with distinct fates — including memory cells.

➡️ Without autophagy, old mitochondria aren’t cleared, the inheritance becomes symmetric, and the diversity in T-cell fates is lost.

➡️ This has major implications for understanding why immune memory weakens with age and may inform new strategies to boost T-cell immunity. 3/Image
Read 6 tweets

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