The COVID-19 pandemic may be over, but our immune systems are still feeling the impact. After years of battling constant viral threats, from COVID-19 to seasonal flu and other infections, our body’s defense system is exhausted. Many people continue to experience lingering inflammation, frequent illnesses, and slower recovery times. This extended state of immune stress has compromised us further to chronic illness, including autoimmune diseases and even neurodegenerative diseases such as Parkinson's. So why is our immune system still in trouble? And how do we give it its power back? Understanding immune exhaustion is the beginning of rebuilding our body's natural immunity.

A weakened immune system makes people more susceptible to disease, mental illnesses, and even sleep disorders. Now, new research indicates that immune system depletion may play an important role in the onset of Parkinson's disease, a degenerative neurologic disorder that compromises movement and cognition.

Role of Inflammation in Parkinson's Disease

Dysfunctional immune response is a leading cause of long-standing inflammation within the body, that has been found to contribute towards a multitude of conditions, including cardiovascular conditions, diabetes, depression, and neurodegenerative diseases such as Alzheimer's.

As people age, their immune system naturally becomes less effective. This deterioration, referred to as immune exhaustion, may be a key contributor to the onset and progression of Parkinson’s disease. Rebecca Wallings, a Parkinson’s Foundation Launch Award grant recipient and senior postdoctoral fellow at the University of Florida, believes that an accumulation of exhausted immune cells could be driving neurodegeneration in Parkinson’s patients.

How a Tired Immune System Might Affect Parkinson's?

Parkinson's disease is most commonly linked with the degeneration and loss of dopaminergic neurons—motor nerve cells that produce dopamine, an essential neurotransmitter for movement. While researchers have long suspected inflammation is involved in this neurodegeneration, the mechanisms are not yet well understood.

Wallings' study is on immune cell exhaustion, a process by which aging immune cells fail to control immune responses effectively. Her research indicates that instead of dampening inflammation in Parkinson's patients, attempts should be made to rejuvenate the immune system to regain its functionality.

Energy Deficiency in Immune Cells

One of the major findings of Wallings' work is the function of mitochondrial impairment in immune cell exhaustion. Mitochondria are commonly called the powerhouses of cells, as they are vital for generating energy. As mitochondria age and become inefficient, immune cells fail to function well, potentially accelerating neurodegeneration in Parkinson's disease.

Wallings has found that mutations in the LRRK2 gene, a recognized genetic risk factor for Parkinson's disease, are linked with defective mitochondrial function and immune cell exhaustion. Her current work includes testing various therapeutic approaches to restore mitochondrial function in immune cells with the potential to enhance the immune system and potentially prevent or treat Parkinson's disease.

Will Rejuvenating the Immune System Help in Treatment?

For decades, the standard practice in treating Parkinson's has been to suppress brain inflammation. Yet Wallings' work indicates that instead of slowing down immune responses, restoring the immune system could be a more successful strategy. By addressing mitochondrial impairment and immune resilience, researchers can potentially reverse or slow down Parkinson's disease.

Wallings is now looking into how to rejuvenate immune cells by fixing mitochondria. She studies immune cells from patients with Parkinson's as well as from healthy subjects and performs experiments on animal models to determine if rejuvenation of the immune system could result in improved disease outcomes.

Lifestyle Factors That May Affect Parkinson's Risk

While there is no cure for Parkinson's disease, some lifestyle adjustments may decrease the chances of developing the illness. Since neurodegenerative diseases are associated with chronic inflammation and immune dysfunction, developing habits that enhance immune function might prove helpful.

Diet: There is evidence to suggest that eating in accordance with the Mediterranean or MIND diets, both high in antioxidants, healthy fats, and anti-inflammatory foods, can encourage brain wellness and reduce Parkinson's risk.

Avoiding Dangerous Substances: Restricting alcohol and nicotine use can maintain a robust immune system and suppress inflammation.

Reducing Stress: Chronic stress weakens immune function, so methods such as meditation, exercise, and sufficient sleep can lead to improved overall well-being.

A new, highly mutated COVID variant called 'Cicada' is spreading in the US. This is the BA.3.2 mutation of the COVID-19 variant. While nationally the cases of COVID have remained low, the BA.3.2 strain is gaining traction across the globe.

What Is The Cicada COVID Variant?

Cicada or the BA.3.2 strain emerged over a year ago, and simmered until last fall. However, this was when it started ramping up in countries including the US. As of February, BA.3.2 has been detected in at least 25 states, noted the US Centers for Disease Control and Prevention (CDC).

The variant's slew of genetic changes in its spike protein is what has made people concerned. This is what makes it unique and distinct from other variants in circulation.

According to Andrew Pekosz, Ph.D., a virologist at the Johns Hopkins Bloomberg School of Public Health, as reported by TODAY.com, "It [the variant] has a lot of mutations that may cause it to look different to your immune system."

The SARS-CoV-2 virus that causes COVID-19 mutates constantly and spreads over time. It thus leads to emergence of new variants.

A new study published in the CDC’s Morbidity and Mortality Weekly Report suggests that emerging variants could weaken protection gained from prior COVID-19 infection or vaccination.

One such “hyper-mutated” strain, BA.3.2, is now being closely tracked by public health officials. In December 2025, the World Health Organization classified it as a “variant under monitoring.”

Read: COVID Variant BA.3.2 Spreads To 23 Countries: Is The Variant Under Monitoring A Cause Of Worry?

When Was Cicada COVID Variant First Detected?

BA.3.2 was first detected in South Africa in November 2024. It is a descendant of BA.3, an Omicron subvariant that appeared in 2022 and briefly circulated alongside BA.1 and BA.2, according to the CDC.

Although BA.3 never became dominant, it did not completely disappear. “It fizzled out, but persisted at low levels,” said Pekosz. After two years and dozens of mutations, BA.3.2 eventually emerged.

For much of 2024, the variant spread quietly, overshadowed by dominant strains like Nimbus and XFG, which stem from BA.2. However, by September, BA.3.2 began gaining ground. “It was under the radar, replicating, until it started spreading more efficiently between people,” Pekosz noted.

What sets BA.3.2 apart is its spike protein, which carries an unusually high number of mutations — around 70 to 75. This makes it significantly different from strains such as JN.1 and LP.8.1, which current COVID-19 vaccines are designed to target.

The CDC describes BA.3.2 as a “genetically distinct” lineage compared to recent variants. Early laboratory studies suggest it may be capable of evading existing immunity, as its spike protein changes help it escape neutralising antibodies.

What Makes Cicada So Unique?

The BA.3.2 variant is nicknamed by T Ryan Gregory, Ph.D., a professor of evolutionary biology at the University of Guelph. He wrote on X, formerly Twitter: "Well, it's that time again. Meet "Cicada", BA.3.2* (including descendant RE.*). This one has been underground for years (its ancestor BA.3 hasn't been circulating since early 2022, and didn't do much then either) but is now emerging as a contender for the next major lineage."

While most of the symptoms of this new variant remains same as from the other variants, one thing that stands out here is the gastrointestinal symptoms that cicada could cause. However, experts note that this variant will not make anyone more sicker. Other symptoms include:

• Cough
• Fever or chills
• Sore throat
• Congestion
• Shortness of breath
• Loss of smell or taste
• Fatigue
• Headache

On March 13, the Ministry of Social Justice and Empowerment introduced the Transgender Persons (Protection of Rights) Amendment Bill, 2026, in the Lok Sabha. Amid opposition, the Rajya Sabha gave its not to the Bill on March 25. The bill seeks to amend the Transgender Persons (Protection of Rights) Amendment Act 2019. The bill was passed in the Lok Sabha on March 24.

What Makes The Bill So Controversial?

What the law originally promised: India's legal framework for transgenders rights comes from the landmark NALSA v. Union of India ruling. This is where the Supreme Court recognized transgender persons as 'third gender' and affirmed their fundamental rights, including access to healthcare. The 2019 amendment followed and promised non-discrimination in education employment, housing, and crucially, healthcare. As per a Live Law analysis, the law was intended to align with constitutional guarantees of equality and dignity, especially under Article 14 (Equality Before Law), 15 (Prohibition of Discrimination), and 21 (Right To Life).

Recent amendments have however raised concerns because of how it could reshape access to healthcare and recognition of identity.

What Does The New Bill Introduce?

The Bill introduces stricter verification of identification and tightens the definition of transgender identity by replacing self-identification with mandatory medical certification. This, many argue is against the 2019 Act supported by the NALSA judgment.

'We, the transgender people of India, reject the erasure of our identity," writes Dr Aqsa Shaikh for the media outlet - The Indian Express. One of the biggest concerns she and many pointed was the continued requirement of official certification for gender identity.

While the law does not always explicitly mandate surgery, activists argue that in practice, access to updated identity documents often becomes tied to medical procedures.

This creates barriers to gender-affirming healthcare, which includes hormone therapy, surgeries, and mental health support.

Dr Shaikh, who is a transgender professor at the Department of Community Medicine in Hamdard Institute of Medical Sciences and Research, Jamia Hamdard, argues that such provisions undermine the principle of self-identification, which was central to the NALSA judgment.

Gaps In Gender-Affirming Healthcare Access

Experts have long pointed out that transgender healthcare in India is already limited:

• Few public hospitals offer structured gender-affirming services
• Mental health support tailored to transgender individuals remains scarce
• Hormone therapy is often accessed informally without supervision

Critics also argue that the amendments do little to expand healthcare infrastructure, focusing instead on administrative control.

Health activists have also flagged the absence of:

• Universal insurance coverage for gender-affirming procedures
• Clear funding commitments for public healthcare services
• Standardized treatment protocols across states

This is significant because transgender individuals face disproportionately high rates of:

• Depression and anxiety
• Substance use disorders
• Suicide risk

Without systemic healthcare guarantees, the law’s protections risk remaining symbolic.

Erasure Of Identity

An opinion piece in The Leaflet describes this bill as an "architecture of erasure". The piece argued that it weakens recognition of diverse transgender identities by reinforcing bureaucratic control. Dr Shaikh argues that the community rejects any framework that takes away the right to self-identify, calling it a rollback of constitutional morality.

Furthermore, a LiveMint report notes that the amendment is a "hurried, short-sighted decision" because it was passed without adequate consultation with transgender communities, it ignores lived experiences and healthcare needs, and prioritizes regulation over welfare.

Live Law notes that any law that govern transgender rights must remain consistent with the NALSA judgment. However, the recent amendment could dilute the principle supported by NALSA judgment that gender identity is based on self-perception and not state or medical approval.

Metformin Brain: A popular diabetes drug, prescribed to manage type 2 diabetes by controlling blood sugar, which has been in use for 60 years - metformin, now shows how it is directly linked to the brain.

A drug used for over six decades did not have a study that made scientists sure of exactly how it works, until now. Researchers from the Baylor College of Medicine in the US were able to identify in 2025 a brain pathway that the drug seems to work through. It also has impacts on biological processes in other areas of the body.

"It's been widely accepted that metformin lowers blood glucose primarily by reducing glucose output in the liver. Other studies have found that it acts through the gut," said Makoto Fukuda, a pathophysiologist at Baylor.

"It's been widely accepted that metformin lowers blood glucose primarily by reducing glucose output in the liver. Other studies have found that it acts through the gut," said Makoto Fukuda, a pathophysiologist at Baylor.

What the Study Found

In a 2025 study on mice, researchers observed that metformin travels to the VMH and switches off Rap1 activity. This action appears to be crucial for its ability to control blood sugar. To test this further, scientists bred mice that lacked Rap1. In these mice, metformin no longer improved diabetes-like symptoms, even though other medications still worked.

This points to something important. Metformin may be working through a completely different pathway compared to other diabetes drugs, one that depends on the brain.

Read: Metformin Controls Blood Sugar With Help From Brain Neurons, Finds Study

The researchers also identified specific nerve cells involved in this process. They found that SF1 neurons become active when metformin enters the brain, suggesting these cells play a direct role in how the drug works.

Why This Matters

These findings could change how doctors and scientists think about diabetes treatment. If metformin’s brain pathway is confirmed in humans, future therapies could be designed to target these exact neurons, making treatments more precise and possibly more effective.

There is also a bigger picture. Metformin has already been linked to benefits beyond diabetes, including slowing aspects of brain aging and improving longevity. In one study involving postmenopausal women, those taking metformin had a significantly lower risk of dying before the age of 90 compared to those on another diabetes drug.

Read: Metformin Can Help Lower Risk Of Age-related Vision Loss: Study

What Comes Next

While the results are promising, human studies are still needed. If confirmed, this discovery could open the door to new treatments that not only manage blood sugar better but also tap into the brain’s role in overall health and aging.

It also reinforces an emerging idea that metformin is not just acting on the body’s metabolic organs, but quietly influencing the brain at much lower doses.