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.

In moments where life seems to slip away, many people describe seeing a bright tunnel with a strong light shining at the end. The image feels almost otherworldly. Whether it happens during major surgeries, car crashes, or sudden accidents, people from different places and backgrounds share accounts that sound strikingly alike. Films, novels, and personal stories often mention this same vision during a near-death experience. While some link it to a glimpse of the afterlife, there may be a scientific explanation for why the mind creates this scene.

Is it a sign of something beyond the physical world, a reaction of the mind in distress, or part of how the brain behaves as it shuts down? Here is what researchers have learnt.

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Do You Really See A Tunnel Of Light When You Die?

Yes. Scientists agree that many people do report seeing a tunnel of light when death is close. Even though death is certain, much about it still feels unclear. For generations, people have tried to understand what takes place in those last moments. Only in recent years, as medical care has advanced, have researchers been able to look more closely at near-death experiences, also known as NDEs, which occur when someone comes dangerously close to dying.

One of the most repeated features of NDEs is the bright tunnel, a sight described by millions. It is not a quick trick of the mind. People often speak of it as deeply emotional and unforgettable. This leads to difficult questions. Does this vision suggest something beyond physical life, or is the brain responding to extreme stress in its final effort to survive?

Why Do You See A Tunnel Of Light During Near-Death Experiences?

When someone nears death, the body begins to change very quickly. Vital functions start to drop. The heart may slow, reducing the amount of oxygen that reaches the brain. Body temperature can fall, and breathing may become weak or uneven. Along with these physical changes, the brain also reacts in its own way.

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Tunnel Of Light During Death Experiences: What Scientists Found

A team at the University of Michigan studied what happens in the brain as a person dies. They examined four people who were removed from life support and found that two of them showed a strong surge of brain activity right before death.

The pattern of activity was similar to what occurs when a person is awake and using higher thought. These bursts were produced by gamma waves, which are linked to conscious processing. In one patient, the rise in gamma activity was nearly three hundred times higher than normal.

Jimo Borjigin of the University of Michigan suggested that this might show a form of hidden awareness that becomes active just before death.

Professor Borjigin explained that some people near death may recall seeing or hearing things or may feel as though they are watching their body from above, or even moving through space. She said her team may have identified the basic brain steps connected to this type of hidden consciousness.

She added that future research needs to involve people who survive such events, so their brain activity can be compared with their own descriptions of what they experienced.

Another study in the Journal of the Missouri State Medical Association also explores how consciousness may shape near-death experiences. The researchers note that there is still much to learn about how the brain creates awareness and how that awareness influences what people see or feel as they approach death.

A team of Indian scientists has uncovered a rare mutation in the USP18 gene that appears to drive repeated neurological deterioration in children. This unusual mutation offers important clues about a disorder previously seen in only 11 cases worldwide, now identified for the first time in India.

The work was carried out by specialists at the Indira Gandhi Institute of Child Health in Bangalore, along with researchers from Ramjas College, University of Delhi, and Redcliffe Labs. But what does this neurological condition involve?

The study, featured in the journal Clinical Dysmorphology, describes a never-before reported variant, c.358C>T (p.Pro120Ser), adding to what is known about Pseudo-TORCH syndrome type 2.

What Is Pseudo-TORCH Syndrome Type 2?

Pseudo-TORCH syndrome type 2 is an extremely uncommon inherited disorder that affects how a child’s brain forms and functions. The symptoms often resemble those caused by congenital infections, though no actual infection is present.

According to the researchers, it is marked by serious brain abnormalities such as intracranial calcifications, a smaller-than-usual head size, and white matter injury. These problems can lead to seizures, stiffness of the limbs, and often early death. The condition results from recessive mutations in genes like USP18.

What Is The USP18 Gene?

The USP18 gene provides instructions for making the Ubiquitin-Specific Peptidase 18 protein, which helps regulate the body’s type I interferon response. It performs two major tasks. It works as an enzyme that removes ISG15 tags from certain proteins, and it also dampens interferon signaling by attaching to the IFNAR2 receptor. Disturbances in this gene are linked to interferon-related disorders and some cancers, according to the National Institutes of Health.

In a healthy state, USP18 keeps the immune response balanced so the body does not produce unnecessary inflammation. When the gene is altered, this control weakens and the immune system reacts in an exaggerated way, which can damage the developing brain.

“The finding shows how clinical experience combined with advanced genetic tools can change outcomes. For years, we treated symptoms without a clear explanation, but identifying this new USP18 mutation has changed both the diagnosis and the child’s path forward,” said Dr. Vykuntaraju K. Gowda from the Department of Pediatric Neurology, IGICH, speaking to IANS.

What Doctors Found?

The investigation began with an 11-year-old girl who had shown symptoms since infancy, including repeated episodes of febrile encephalopathy, meaning fever-associated unconsciousness, along with seizures, developmental delays, and microcephaly. Her brain scans over time showed growing calcium deposits in several regions.

To trace the cause of her recurring neurological episodes, the doctors advised detailed genetic analysis. Using exome sequencing combined with mitochondrial genome testing, the team uncovered a previously unknown alteration in the USP18 gene, finally providing an explanation after years of uncertainty.

This new mutation changes the USP18 protein’s shape, reducing its ability to keep inflammation under control. The overly active immune response offers a clear reason for the child’s repeated fever-linked neurological decline. Recognising this link is important because it helps clinicians spot early signs, avoid unnecessary infection-related treatments, and pay closer attention to conditions caused by immune overactivity instead.

“This is also the first reported instance of a USP18-related disorder showing up as recurrent febrile encephalopathy,” said Dr. Himani Pandey, part of the research team.

The study underscores the value of early genetic testing in children with unexplained neurological issues and suggests new possibilities for more focused care in the years ahead.

In a breakthrough investigation published in Nature Medicine found that GLP-1 medicines are not just weight loss drugs, but actually brain reprogramming drugs. The study highlighted how deeply GLP-1 medications influence our brain's reward circuits, cravings, and the electrical rhythm.

Case Study

The study took a 60-year-old woman who had a lifelong "food noise", and underwent deep-brain stimulation that targeted the nucleus accumbens, which is brain's craving centre. The woman was also to start tirzepatide, an antidiabetic medication used to treat type 2 diabetes and for weight loss, which is an active ingredient in Mounjaro. As she reached her full dose, her compulsive food thoughts went silent, however, five to seven months later, the neutral signal returned before her cravings did, while she was still on the medication.

How Was The Study Conducted?

Scientists from the University of Pennsylvania, monitored brain activity directly from the nucleus accumbens in people using tirzepatide.

The research followed three patients with severe food preoccupation and uncontrolled eating. Two underwent deep-brain stimulation, while the third received tirzepatide and also had electrodes implanted around the same time. When cravings or intense food thoughts occurred, researchers observed strong delta-theta waves in the nucleus accumbens. These slow brain signals are linked to reward, motivation, and compulsive eating.

Once the patient on Mounjaro reached the full therapeutic dose, the changes were dramatic: for nearly four months, they reported almost no episodes of “severe food preoccupation.” Their delta-theta activity also fell to very low levels, even during moments when cravings typically occurred. However, while initially there was a suppression in the brain activity that triggered cravings, the cravings returned over time.

Why Does This Matter?

This is the first time scientists have been able to directly record craving-related brain activity in real time and compare it before and after using a medication like Mounjaro. Although the study involved only three people, the findings help explain why medications in this class appear to influence more than just appetite. They may also reshape how the brain processes reward and desire around food.

The researchers say larger studies are needed, but early signs point to a clearer understanding of how obesity drugs change both behavior and brain biology.

What To Keep In Mind?

Dr Simon Cork, senior lecturer in Physiology, Angila Ruskin University said that there must be some caution that should be applied while looking at the findings of the study.

Dr Cork says, "This study specifically looked at a marker of brain activity associated with periods of “binge eating” in patients with obesity associated with food preoccupation. This is important because this is a specific (and rare) condition associated with obesity. They found that in three patients, periods of intense preoccupation with food was associated with a characteristic change in brain activity in a region of the brain associated with reward...While this study is methodologically very interesting, it has to be clear that this is only one patient with a very specific condition that is associated with obesity and so shouldn’t necessarily be generalised to the entire population.”