Aging in India

The United Nations Population Division estimates the number of people aged 65 and older will double over the next three decades, reaching 1.6 billion by 2050. As more people are living longer, they are more likely to have two or more persistent chronic conditions, also known as multimorbidity. This makes it difficult for patients to manage their health and can strain health system resources.

A recent study led by Preeti Zanwar, PhD, MPH, MS, an adjunct research and teaching faculty and aging and health disparities researcher at Jefferson, sheds light on the prevalence of multimorbidity among aging adults in India and recommends how public health officials can prevent adverse effects.

Dr. Zanwar reviewed data from the Longitudinal Aging Study of India, the largest nationally representative longitudinal survey study of adults in India and found that multimorbidity is prevalent across various sub-populations in India, including older adults, women, those within groups of lower socioeconomic status and Muslims. The study found that these populations had a higher burden of chronic conditions such as diabetes, obesity, cardiovascular diseases, stroke and cancer.

Dr. Zanwar says results need to be taken with caution given that multimorbidity prevalence in this study is self-reported and only captured among those who had access to a healthcare professional. Nevertheless, these findings emphasize the urgent need for public health interventions to prevent, manage and control multimorbidity among older adults in India and other countries.

“It is a global issue,” Dr. Zanwar says. “This is an important time for researchers to do cross-country comparisons on multimorbidity and the policies that can help address this issue.”

To Dr. Zanwar’s surprise, the study found that multimorbidity rates were higher than expected among individuals with higher levels of education. Future research could investigate the role of education as a risk or protective factor for multimorbidity.

The study suggests greater access to health care, care coordination among providers and culturally tailored interventions as essential strategies to address the growing multimorbidity prevalence in India and reach those who may not have access to care.

By Queen Muse

Gut Protein May Protect Brain Cells in Parkinson’s Disease

Nearly 10 million people worldwide suffer from Parkinson’s Disease (PD), a condition causing muscle rigidity and tremors due to the loss of the chemical dopamine in the brain. One cause of PD is exposure to toxins. In a recent study, Scott A. Waldman, MD, PhD, and his team discovered that a gut receptor protein called GUCY2C could prevent PD development by protecting against brain damage and toxic insult.

Dr. Waldman’s team has been studying GUCY2C, for years. It’s generally known for its role in water and salt secretion in the gut. However, GUCY2C is also produced in the brain. Previously, the team removed GUCY2C from gut cells in mice and saw an increase in the expression of genes associated with PD. “That’s when we made that leap from the gut to the brain,” says Dr. Waldman. “If we removed GUCY2C in the brain, would it impact susceptibility to PD?”

Lara Cheslow, an MD-PhD student in the Waldman lab, worked with Richard Smeyne, PhD, chair of the neuroscience department and director of the Jefferson Comprehensive Parkinson’s Disease and Movement Disorder Center, to investigate this question. They found that mice in which GUCY2C expression was “knocked out” or removed had more brain-cell damage and were more susceptible to toxins, compared to mice with normal GUCY2C.

Moreover, when mice with normal GUCY2C levels were exposed to a toxin, GUCY2C levels naturally increased. This suggests that it was almost as if GUCY2C played a protective role in mouse brain cells or neurons, which surprised researchers given its normal role in the gut.

This led the team to look at human samples to see if GUCY2C expression showed the same trends. Samples from PD patients showed elevated GUCY2C levels compared to samples from patients who did not have PD – a result that puzzled researchers.

Current therapies for PD mimic dopamine, which simply manages PD symptoms. Targeting GUCY2C could be a more promising avenue to potentially prevent disease progression altogether by protecting against neuron damage. Although these studies are in the early pre-clinical stages, Dr. Waldman hopes that they can one day benefit patients suffering from PD.

By Moriah Cunningham

Repurposing FDA-approved Drugs May Decrease Fibrosis in Butterfly Disease

“Recessive Dystrophic Epidermolysis Bullosa (RDEB) is the worst disease you’ve probably never heard of,” says dermatology researcher, Andrew South, PhD. RDEB patients and their families know just how horrible it can be. Epidermolysis bullosa (EB) diseases such as RDEB are a rare group of skin blistering diseases that also increase fibrosis, or scarring. Fibrosis is a normal part of the wound healing process. However, in RDEB patients, frequent skin sores lead to a buildup of scar tissue, causing the skin to become even more fragile with every injury.

Dr. South’s lab has been working on ways to delay fibrosis in RDEB, sometimes called ‘butterfly disease.’ In the group’s most recent study, Grace Tartaglia, PhD, a recent graduate from Dr. South’s lab, and colleagues, used a drug screen to investigate FDA-approved drugs that could be repurposed to delay fibrosis in RDEB patient tissue samples. This unbiased approach revealed three major drug categories: kinase inhibitors and steroids, which were already known to decrease fibrosis, and a third surprising class of drugs – antivirals.

Considering no one previously studied antivirals to treat fibrosis in RDEB, the team explored this therapy further. They found that the antiviral with the strongest anti-fibrotic properties was the drug Daclatasvir, which was originally developed to treat patients with hepatitis C. When the researchers treated mouse models of RDEB with Daclatasvir, they saw fibrosis decrease and activity and lifespan of the mice increase.

The lab is now working to understand how the mechanism of how an antiviral can decrease fibrosis, and some of their previous studies have generated hypotheses for them to test. They are also looking to see if the results with Daclatasvir they saw in mice can be replicated in RDEB patients. They are teaming up with Neda Nikbakht, MD, PhD, who leads Jefferson’s EB Adult Clinic to start. “We really need support from clinicians around the country,” Dr. South stresses. “We are looking for clinical centers with enough RDEB patients to work on a Daclatasvir clinical trial with us.”

By Moriah Cunningham