For over 15 years, Dr Anthony Shum, a pulmonologist at the University of California, San Francisco has been studying a rare genetic disorder called the COPA Syndrome. It stands for coatomer subunit alpha and is a rare, inherited disorder that affects the lungs, joint, and kidney. The National Organization for Rare Disorder also notes that it is a genetic autoimmune disorder that is caused by mutations in the COPA gene. This disease affects families unpredictably—some individuals with the mutation develop severe lung damage early in life, while others remain completely healthy. Now, Shum’s team has discovered a protective genetic variant that may offer new hope for treatment.

A Breakthrough

Researchers found that some relatives of COPA Syndrome patients stayed healthy despite carrying the same COPA gene mutation that causes the disease. The key difference? These unaffected individuals had a protective version of another gene called HAQ-STING.

When scientists introduced HAQ-STING into diseased lung cells from COPA patients, the cells returned to a balanced state, suggesting that this gene could be used as a therapy.

“We really think HAQ-STING could be a gene therapy tool and a step toward a cure,” said Shum, whose findings were published in the Journal of Experimental Medicine.

Families Who Solved The Mystery

Shum’s journey into COPA Syndrome research began in 2011 when he treated a young woman, Letasha, who had severe lung bleeding. Her mother, Betty Towe, mentioned that Letasha’s sister, Kristina, had suffered from similar symptoms. Over the years, Betty had taken both daughters on a four-hour trip to UCSF for treatment. After tracing their family history, Shum discovered that their distant relatives in Texas and Oakland also had lung problems and arthritis. In 2015, Shum, along with scientists from Baylor College of Medicine and Texas Children’s Hospital identified the COPA gene mutation. They realized that it was the common factor behind the illness. However, only some of the 30 individuals with the mutation actually developed symptoms, leaving a major question unanswered.

The Domino Effect

It was established that it occurs when a mutated COPA gene causes another gene STING to go overdrive. The STING that helps fight infections in COPA patients, remain permanently active, which leads to chronic inflammation that damages the lungs, kidneys, and joints. In 2020, while studying STING’s role in the disease, researchers discovered a key variation: HAQ-STING. This version of STING, present in about one-third of the population, appeared to neutralize the harmful effects of the COPA mutation.

To confirm their theory, the scientists needed both affected and unaffected family members to participate in the testing. Letasha, Kristina and Betty immediately volunteered. The researchers then analyzed DNA samples from 26 COPA patients and their healthy relatives. They also conducted CT scans and blood tests to ensure that unaffected members did not have any hidden symptoms. When the findings were all clear, it was revealed that all the healthy individuals had HAQ-STING, while none of the COPA patients did. This was the first known case of a common gene variant completely protecting against a severe genetic disease.

Encouraged by this discovery, researchers tested HAQ-STING’s effects in a lab setting. They introduced it into diseased lung cells from COPA patients, and the cells returned to normal function.

Way Ahead

Shum believes HAQ-STING could lead to game-changing treatments, including:

• Prenatal gene therapy for babies diagnosed with COPA Syndrome before birth
• Aerosol delivery of HAQ-STING for adults, directly targeting the lungs

Before publishing their findings, Shum called Betty with the news—her own HAQ-STING gene had protected her from the disease. He also informed Letasha and Kristina, who were overwhelmed with relief and joy.

“We always believed Dr. Shum would get to the bottom of it,” said Letasha. “This discovery is going to change lives.”

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.

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.

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."