Vipin M. Vashishtha Profile picture
Jan 15 13 tweets 4 min read Read on X
Air pollution causing brain damage of young kids!

Tissues from the brains of kids living in Mexico City show features linked to Alzheimer's disease: amyloid-ß plaques, neuronal phosphorylated tau protein tangles & frontal pyramidal immunoreactivity of DNA-binding protein 1/ Image
Furthermore, the city children, with no other risk factors for brain disorders, performed comparatively poorly on cognitive tasks. 2/
It’s well established that air pollution, in the form of particulate matter, ozone or other toxic gases, contributes to asthma, lung cancer and other respiratory illnesses, and that particulate matter especially contributes to heart disease. 3/ Image
Studies have shown that higher levels of air pollution are correlated with increased risks of dementia, as well as higher rates of depression, anxiety & psychosis. Researchers found links to neurodevelopmental conditions, such as autism & cognitive deficits in children. 4/ Image
Neuroimaging revealed that many more children living in the highly polluted city had lesions in the white-matter tracts that connect brain regions than did children in less-polluted areas, with the prefrontal cortex seeming particularly vulnerable. 5/ Image
A recent 16-year study of >200,000 residents in Scotland found that higher cumulative nitrogen dioxide exposure was associated with increased hospital admissions for mental-health and behavioural disorders 6/ Image
Meanwhile, studies in France, the United States and China have documented that in regions where air quality has improved, there are decreased rates of dementia, cognitive decline and depression in older populations. 7/
Few studies have also linked air pollution to structural changes in the brain, such as reduced hippocampal volume, that are consistent with heightened dementia risk in older adults. 8/ Image
Mice exposed to ultrafine particles during development — including in the womb, from their mothers’ breathing — have enlarged white-matter tracts and brain ventricles. Mice exposed during development went on to exhibit greater impulsivity and short-term memory deficits. 9/ Image
In older animals, air pollution seems to accelerate the deposition of the amyloid and tau proteins associated with Alzheimer’s disease. Other animal studies have found damage at the anatomical, cellular and molecular levels. 10/ Image
Brain scans show areas of reduced cortical thickness (coloured regions) in children exposed to higher levels of traffic pollution during their first year of life. 11/ Image
Although signs of damage vary from study to study, Caleb Finch, who researches ageing at the University of Southern California, says that there is one shared facet: “It’s an inflammatory response”. 12/ Image
Studies show that the genes that mediate inflammatory responses are switched on;
messengers associated with inflammation become more abundant; there are signs of oxidative stress & microglial cells that sense damage & protect neurons are activated 13/13

nature.com/articles/d4158…

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More from @vipintukur

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
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

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