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…

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More from @vipintukur

Nov 18
A new study provides some of the strongest evidence yet that mitochondrial dysfunction can directly cause #Parkinson’s disease, rather than being a consequence of neuron loss.

➡️ Researchers used a unique mouse model carrying a mutation in CHCHD2, a mitochondrial protein linked to a rare inherited form of Parkinson’s that closely mimics the common, late-onset form. 1/Image
Key Findings

➡️ Mutant CHCHD2 accumulates in mitochondria, making them swollen and structurally abnormal.

➡️ Cells shift away from normal energy production and develop oxidative stress due to buildup of reactive oxygen species (ROS).

➡️ Alpha-synuclein aggregation occurs after ROS rises, suggesting oxidative stress triggers Lewy body formation.

➡️ Human brain tissue from people with sporadic Parkinson’s showed CHCHD2 accumulation inside early alpha-synuclein aggregates, confirming relevance beyond the rare genetic form. 2/Image
Implications

➡️ This work maps a step-by-step causal chain:
CHCHD2 mutation → mitochondrial failure → metabolic shift → ROS buildup → alpha-synuclein aggregation → Parkinson’s pathology

➡️ It supports the idea that mitochondrial defects may underlie many forms of Parkinson’s, not just the inherited type.

➡️ Targeting oxidative stress, mitochondrial health, and energy pathways could offer new therapeutic strategies. 3/Image
Read 4 tweets
Nov 8
New research in Cell Reports Medicine helps explain why women are more likely to develop #LongCOVID — and often experience more severe, persistent symptoms like fatigue, brain fog, and pain.

The key? Differences in the immune system, gut, and hormones. 1/ Image
Researchers studied 78 people with LongCOVID (mostly mild initial cases) and compared them to 62 who recovered fully.

➡️ One year later, women with Long COVID showed clear biological differences — especially signs of gut inflammation and “leakiness.” 2/ Image
The study also found anemia and hormone imbalances.
Women with LongCOVID had lower testosterone — a hormone that normally helps control inflammation.

➡️ Lower testosterone was linked to more fatigue, pain, brain fog, and depression. 3/ Image
Read 6 tweets
Oct 27
Urine tells the story of #LongCOVID:

➡️ New study identifies a molecular fingerprint for #LongCOVID (PASC) — using just a urine test.

➡️ Researchers found 195 urinary peptides that can accurately distinguish Long COVID patients from healthy and ME/CFS controls (AUC > 0.95). 1/ Image
Researchers used urinary peptidomics to identify a molecular fingerprint of post-acute sequelae of SARS-CoV-2 infection (PASC or LongCOVID).

➡️ Methods

-50 PASC patients (10 months post-infection) were compared with 50 controls (42 healthy + 8 with non-COVID ME/CFS).

-Capillary electrophoresis–mass spectrometry (CE–MS) was used to analyze urinary peptides.

-A support vector machine (SVM) model was built to distinguish PASC cases from controls. 2/Image
➡️ Results

-195 urinary peptides showed significant differences between PASC and controls.

-Most peptides were fragments of collagen alpha chains, suggesting altered collagen turnover, inflammation, and endothelial injury.

-The classifier, named #PASC195, achieved excellent diagnostic performance:
•AUC = 0.949 (training)
•AUC = 0.962 (validation)

-Computational analyses suggested potential benefits from exercise, GLP-1 receptor agonists, and mineralocorticoid receptor antagonists (MRAs). 3/Image
Read 5 tweets
Oct 22
Understanding Long COVID

➡️ Long COVID isn’t one disease — it’s a complex web of immune, vascular, and metabolic dysfunctions.
From fatigue & brain fog to heart & lung complications, it stems from viral persistence, autoimmunity, and mitochondrial damage. 1/ Image
Proposed mechanisms:

1️⃣ Persistent viral reservoirs or antigen remnants

2️⃣ Reactivation of latent viruses (e.g., EBV)

3️⃣ Immune dysregulation & autoimmunity

4️⃣ Endothelial injury and microclots

5️⃣ Gut microbiome imbalance

6️⃣ Mitochondrial dysfunction and energy metabolism impairment. 2/Image
Current management:

- largely symptomatic—rehabilitation, pacing, and supportive therapies.

-Emerging treatments: under study — antiviral drugs, immune-modulating agents, microbiome restoration, and mitochondria-targeted therapies.

-Vaccination: reduces risk and severity of LongCOVID. 3/Image
Read 5 tweets
Oct 22
Fathers’ COVID & offspring

➡️ New research shows that paternal SARS-CoV-2 infection before conception can alter sperm RNA — leading to anxiety-like behavior & brain gene changes in offspring.

A biological “memory” of infection may pass across generations. 1/ Image
Beyond infection: inheritance

➡️ Male mice infected with SARS-CoV-2 fathered pups with altered hippocampal transcriptomes & higher anxiety.
Injecting sperm RNA from infected males reproduced the same effects — clear evidence of RNA-based inheritance. 2/ Image
COVID’s unseen legacy

➡️ Study suggests COVID infection in fathers may have transgenerational effects via changes in sperm small RNAs.
Adds a new layer to how pandemics shape health — not just for one generation, but possibly the next. 3/ Image
Read 4 tweets
Oct 13
A new study provides new evidence to help us redefine steroid use in TB care

➡️ Given the renewed interest in the steroid dexamethasone, as a host-directed treatment during the COVID-19 pandemic, the Trinity College Dublin team provides evidence that treating patients with steroids may enhance the function of their macrophages to kill the mycobacteria, while diminishing pathways of inflammatory damage. 1/Image
The researchers goal was to determine whether dexamethasone impacts the macrophage's ability to fight TB. Although glucocorticoids can reactivate TB, they are paradoxically the only adjunctive host-directed therapies that are recommended by WHO for TB.

Steroids are given to patients alongside antimicrobials in certain circumstances; however, scientists don't fully understand the effect of these drugs on the immune system, especially innate immune cells such as macrophages. 2/Image
The researchers studied macrophages derived from the blood of healthy volunteers or isolated from lung fluid donated by patients undergoing routine bronchoscopies.

➡️ By treating and infecting these macrophages in the lab with Mtb, the scientists could examine and understand how dexamethasone affects the immune response that protects the lungs during infection. 3/Image
Read 9 tweets

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