A 'Tired' Immune System Could Be A Latent Trigger For Parkinson’s Disease

Updated Mar 1, 2025 | 09:25 AM IST

SummaryParkinson’s disease affects over 10 million people worldwide, with 60,000 new cases diagnosed annually in the U.S. Research suggests immune system exhaustion and chronic inflammation may contribute to neurodegeneration in Parkinson’s patients.
Is A 'Tired' Immune System The Hidden Trigger For Parkinson’s Disease?

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.

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Alzheimer's Sleep Loss May Be Reversible; Study Sparks Hope For New Treatments

Updated Jul 28, 2026 | 09:00 PM IST

SummaryAccording to new research, sleep loss, one of the earliest and most challenging symptoms of Alzheimer's disease, could be restored successfully.
Alzheimer's Sleep Loss May Be Reversible; Study Sparks Hope For New Treatments

Credit: AI

Sleep disturbances are among the most debilitating symptoms of Alzheimer’s disease. It often appears years before significant memory decline and other symptoms.

A new study from researchers at the University of Kentucky suggests that this sleep loss may not be permanent.

Instead, it could be driven by an immune response in the brain that may be reversible, sparking hope for new treatments.

Published in the journal Alzheimer’s & Dementia, the study found that brain immune cells called microglia, rather than amyloid plaques themselves, are the primary cause of sleep disruption in Alzheimer’s disease.

In mouse-based trials, researchers were able to restore more than two hours of sleep per day by temporarily removing these immune cells, without reducing amyloid plaques.

Can Sleep Be Restored In Alzheimer’s Patients?

For years, scientists believed that sleep problems in Alzheimer’s were caused by the accumulation of amyloid plaques or the gradual death of brain cells. However, this study points in a different direction.

Researchers discovered that when amyloid plaques begin forming in the brain, they activate microglia, the brain’s resident immune cells.

Instead of protecting the brain, these cells cause inflammation that keeps brain circuits active, preventing sleep.

Using a drug called pexidartinib (PLX3397), the researchers temporarily depleted around 87% of microglia in Alzheimer’s mouse models.

This restored over two hours of daily sleep, particularly non-rapid eye movement (NREM) sleep, which is essential for tissue repair, memory strengthening, and clearing waste products from the brain.

Notably, the improvement occurred without changing amyloid plaque levels, suggesting that inflammation is manageable.

Also read: Captain ‘Sully’ Sullenberger, ‘Miracle On The Hudson’ Pilot, Reveals Early-Stage Alzheimer’s Diagnosis

'Paradigm Shifting' Findings

Lead researcher Dr. Shannon L. Macauley, associate professor of physiology at the University of Kentucky College of Medicine, said, “Basically, we showed that it is not the plaques themselves, or solely dysfunctional neurons, that cause sleep loss but actually microglia.

Microglia are immune cells that, when they respond to plaques, kick off this elaborate cascade of inflammation, as if the microglia are partying all night, and keeping the brain awake.”

She also highlighted why losing restorative sleep can accelerate disease progression.

“That restorative sleep is super important for physical repair, learning and memory and washing out the toxins of the day. When Alzheimer’s patients lose this stage, they lose their brain’s primary cleaning cycle, creating a feed-forward loop that may drive further damage,” she explained.

First author Dr. Nicholas J. Constantino said one of the biggest surprises was that sleep problems did not worsen as amyloid plaques increased.

“I expected that as plaque burden became more severe, sleep disruption would also worsen. The disruptions in sleep… did not worsen by 18 months, despite more than double the amount of plaque burden,” Constantino said.

Also read: What Is Type 3 Diabetes? Insulin Resistance In The Brain That Could Trigger Alzheimer’s

Why Do Alzheimer’s Patients Lose Sleep?

Poor sleep and Alzheimer’s create a vicious cycle. Sleep deprivation reduces the brain’s ability to clear amyloid-beta and tau proteins, which can accelerate disease progression, while worsening sleep.

Sleep disturbances affect up to half of people living with Alzheimer’s disease. The disease disrupts sleep due to various reasons:

Overactive microglia: As shown in the new study, immune cells become chronically activated by amyloid plaques, releasing inflammatory signals that keep the brain in a heightened state of activity.

Damage to sleep-regulating brain regions: Alzheimer’s progressively affects areas like the hypothalamus and brainstem that regulate the sleep-wake cycle.

Loss of NREM sleep: Due to lack of deep sleep, the brain’s ability to clear metabolic waste, including amyloid plagues weakens.

Circadian rhythm disruption: Degeneration of the brain’s internal clock leads to broken sleep and daytime drowsiness. This fuels confusion and agitation associated with the disease.

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Not Just The Heart, Obesity In Midlife Could Be Just As Harmful To The Brain: Study

Updated Jul 28, 2026 | 07:07 PM IST

SummaryA recent study has found that obesity in late adulthood can lead to faster brain ageing and subsequent cognitive decline.
Can Obesity Lead To Long-Term Cognitive Decline? Scientists Discover Evidence

Credit: AI

Obesity has always been considered as one of the contributors to heart disease, diabetes, and stroke.

Now, growing research suggests that excess body fat, particularly in your 40s and 50s, may also accelerate brain aging and raise the risk of long-term cognitive decline.

Researchers say that obesity is not just linked with memory problems but also to significant changes in the brain structure.

Maintaining a healthy weight, especially during midlife, could help prevent memory problems and overall cognitive decline.

Higher BMI Linked To Faster Brain Aging

A recent study by researchers at the University of Georgia followed more than 8,200 adults aged 50 years and older for nearly 24 years.

The researchers found that individuals whose body mass index (BMI) increased over time experienced faster declines in cognitive performance than it would with normal aging. Excess body weight affected several aspects of cognition, including memory, planning, decision-making, problem-solving, emotional regulation, and concentration.

Lead author Dr. Claire Sexton (University of Georgia College of Public Health) said, "Maintaining a healthy body weight throughout adulthood may be an important strategy for preserving cognitive health later in life."

The study adds to the evidence that preventing weight gain throughout adulthood could become crucial for reducing dementia risk.

Also read: Grade-1 Fatty Liver: More Indians Are Developing It at Lower BMIs. What's Behind the Shift?

How Does Obesity Affect The Brain?

Chronic Inflammation

Obesity causes chronic low-grade inflammation, which can potentially damaging neurons essential for learning and memory.

Insulin Resistance

The brain relies on glucose for energy. Insulin resistance, common in obesity, may impair how brain cells use glucose, affecting memory and thinking.

Reduced Blood Flow

Obesity increases the risk of hypertension, atherosclerosis and vascular disease, reducing blood supply to brain tissue and potentially accelerating cognitive decline.

Visceral Fat

Experts believe visceral fat, the fat surrounding internal organs, may be more damaging than body weight alone. It produces inflammatory chemicals linked to brain changes and dementia risk.

Also read: Beyond Weight Loss: Scientists Discover How Exercise Can Help Reverse Muscle Aging

Growing Evidence

The latest findings are supported by several years of research. A large review published in Practical Neurology concluded that obesity is associated with smaller hippocampal volume, temporal lobe atrophy, mild cognitive impairment and increased Alzheimer's disease risk.

Some studies have suggested that obesity during midlife may nearly double the risk of developing Alzheimer's disease or dementia later in life.

Another review on obesity and aging reported that higher BMI is associated with poorer verbal memory, slower information processing and reduced executive function, particularly among older adults.

In January 2026, researchers also used genetic analyses to suggest that obesity and high blood pressure may directly contribute to dementia.

Can The Risk Be Reduced?

With a few lifestyle improvements, overweight and obese individuals can maintain a healthy BMI, reducing the risk of faster brain ageing and cognitive degradation. Experts recommend focusing on overall metabolic health rather than the number on the weighing scale alone.

Maintaining a healthy weight, regular exercise, controlling blood pressure, cholesterol and diabetes, following a Mediterranean diet, getting adequate sleep, remaining socially and mentally active can help maintain a healthy body weight.

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World Hepatitis Day: Living With Someone Who Has Hepatitis? Experts Reveal If You're At Risk Of Getting Infected

Updated Jul 28, 2026 | 04:08 PM IST

SummaryNot all types of hepatitis is spread through blood or bodily fluids exposure. Experts decode what kind of hepatitis is transmitted in close quarters.
World Hepatitis Day: Living With Someone Who Has Hepatitis? Experts Reveal If You're At Risk Of Getting Infected

Credit: AI

Living with someone who has hepatitis can be worrying. People tend to immediately wonder whether they are at risk simply by sharing meals, hugging, or living under the same roof.

Fortunately, the answer depends on the type of hepatitis, and in most cases, everyday household contact does not spread the virus.

Dr. Shalimar, Prof. Department of Gastroenterology, AIIMS explains, "Hepatitis means inflammation of the liver. There can be many causes, but viral hepatitis is one of the most common. There are different hepatitis viruses, including A, B, C, D, and E. Some cause acute illness, while others can lead to long-term liver damage, including cirrhosis and liver cancer."

Experts say misinformation surrounding hepatitis often leads to unnecessary fear and stigma, causing patients to feel isolated. Understanding how different hepatitis viruses spread can help families protect themselves without avoiding normal interactions.

Can You Get Hepatitis By Living With Someone?

Dr Nanda Kishore M, Gastroenterology, Athulya Geriatric Care Hospital, answers our question, "No, Hepatitis is not a communicable disease that spreads through everyday contact such as hugging, holding hands, coughing, or sneezing."

For most forms of hepatitis, the answer is no. However, hepatitis B is spread through contact with infected blood and certain body fluids. Household transmission is possible, but it generally occurs when infected blood enters another person's bloodstream.

Possible household risks include sharing:

  • Razors
  • Toothbrushes
  • Nail clippers
  • Glucose monitoring devices
  • Any item contaminated with blood

Also read: Can Hepatitis Be Completely Cured? Understanding What Treatment Can Achieve

Dr. Kishore says that the mode of transmission largely depends on the type of hepatitis infected.

He says, "Hepatitis A and E are predominantly spread via means of contaminated food and water, while Hepatitis B and C are transmitted through infected blood and certain bodily fluids."

Hepatitis B is preventable by vaccine. Household members of someone with chronic hepatitis B are usually advised to get tested and vaccinated if they are not already immune.

Dr. Shalimar says, "For hepatitis B, current treatment controls the infection, and newer therapies under development offer hope for a functional cure in the future. Vaccination has dramatically reduced hepatitis B in many parts of the world. Expanding vaccination coverage remains one of the most effective ways to prevent the disease."

Living with a hepatitis infected individual is generally safe given that basic hygiene and recommended precautions are followed strictly. Understanding these facts helps reduce unnecessary fear and stigma associated with it.

Also read: Grade-1 Fatty Liver: More Indians Are Developing It at Lower BMIs. What's Behind the Shift?

Importance of Screening & Prevention

Living with someone who has hepatitis does not mean you need to keep your distance. Instead, focus on practical precautions:

  • Never share personal items that may come into contact with blood.
  • Cover cuts and wounds.
  • Wear disposable gloves while cleaning blood spills.
  • Practice good hand hygiene.
  • Ensure hepatitis B vaccination if recommended.
  • Attend regular medical follow-ups if advised by your healthcare provider.

Dr. Ankur Jain, Associate Director & Unit Head, Gastroenterology, Hepatology & Endoscopy, Max Hospital, Dwarka, explains, "Hepatitis B and Hepatitis C continue to affect millions of people worldwide and remain major causes of liver cirrhosis and liver cancer. Individuals with a history of blood transfusions before routine screening, unsafe injections, or other risk factors should discuss screening with their physician.

He adds, "The liver has an extraordinary capacity to heal, but only if we identify problems early and address the underlying causes. Prevention, timely screening, and simple lifestyle modifications remain our most powerful tools in reducing the growing burden of liver disease in India."

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