The team believes that with proper human trials and safety checks, both the miRNA-based therapy and honokiol could go beyond just managing symptoms — they might actually cure Alzheimer’s, or at least stop it in its tracks.
Published Aug 08, 2025 | 4:19 PM ⚊ Updated Aug 08, 2025 | 4:19 PM
Alzheimer's onset. (Creative commons)
Synopsis: New research explored how specific RNA molecules and a compound found in Magnolia tree bark can target brain inflammation and nerve cell death — key drivers of Alzheimer’s. The team also found that the compound could be used as a potential drug.
Alzheimer’s disease (AD), a condition that slowly erodes memory and mental function, may soon have a breakthrough path — not just for treatment, but potentially for a cure.
Indian scientists have identified a promising new therapeutic approach involving RNA — a molecule that carries genetic information and facilitates protein synthesis — and a tree-based compound. This discovery could fast-track drug development and bring new hope to millions.
The research, led by scientists from the Jawaharlal Nehru Centre for Advanced Scientific Research (JNCASR) in Bengaluru and supported by experts from the Manipal Academy of Higher Education (MAHE), explored how specific RNA molecules and a compound found in Magnolia tree bark can target brain inflammation and nerve cell death — key drivers of Alzheimer’s.
Alzheimer’s, which makes up 70 to 80 percent of all dementia cases, is the fifth leading cause of death globally and is expected to rise sharply in the coming years. The disease is marked by abnormal protein clumps in the brain, leading to memory loss, confusion, and cognitive decline.
Currently, there are very few therapeutics available in the market, most of which provide only temporary relief. Recently, a few antibody-based drugs have been approved, but they offer limited benefits to patients.
While the role of various proteins in the development and progression of AD has been well studied, the role of microRNAs (miRNAs) — the discovery of which received the Nobel Prize in Physiology or Medicine last year — in AD is poorly understood.
Think of the brain like a factory, where genes are like instruction manuals and proteins are the workers who get jobs done. For years, scientists have studied the “workers” — the proteins — to understand what goes wrong in Alzheimer’s. However, what if the problem lies with the managers — the ones quietly giving orders behind the scenes? That’s where miRNAs come in.
These tiny molecules don’t make proteins themselves, but they control which proteins get made, when, and how much — like silent supervisors.
Addressing this, researchers from JNCASR, an autonomous institute of the Department of Science and Technology (DST), explored altered miRNAs in the AD brain and also probed the potential of miRNAs to be biomarkers for early, specific and accurate clinical diagnosis of AD.
Using genetically modified mice that mimic Alzheimer’s, scientists Madhu Ramesh and Professor Thimmaiah Govindaraju studied changes in these miRNAs inside the brain. They found several that were “switched on” or “off” in Alzheimer’s brains compared to normal ones — like finding that some managers had started giving the wrong instructions, potentially triggering the disease.
Published in NAR Molecular Medicine, their research zeroed in on one miRNA in particular — called miR-7a. This miRNA controls a powerful protein named Klf4, which in turn affects many genes tied to brain health.
The team found that miR-7a was unusually active in Alzheimer’s, and that it played a key role in sparking neuroinflammation — a kind of chronic fire in the brain that damages cells — and a type of cell death involving iron, known as ferroptosis.
To counter this, the researchers developed two potential treatments. First, they created a synthetic version of miR-7a, called a mimic, which tones down Klf4 and calms the inflammation. Second, they used a natural compound called honokiol.
Honokiol is a natural product found in bark and seed cones of the Magnolia tree that targets Klf4 to stall neuroinflammation and ferroptotic cell death involved in AD. This demonstrates that the miR-7a-Klf4 axis is a novel target for AD and warrants further exploration to develop better therapeutics for the disease.
“The current study offers valuable insight into Alzheimer’s disease by uncovering the regulatory role of miR-7a in controlling neuroinflammation and ferroptosis via Klf4 targeting,” Professor T Govindaraju, one of the researchers involved in the study, said in a statement.
The scientists found that miR-7a acts like a brake on a harmful protein called Klf4, which plays a major role in triggering inflammation and brain cell death in Alzheimer’s. By slowing down Klf4, miR-7a helps protect nerve cells from damage. It does this by calming down inflammation — the body’s internal fire alarm — and preventing a specific kind of rust-like damage to brain cells caused by iron, known as ferroptosis.
What’s promising is that the team also found that honokiol targets the same dangerous pathway and could be used as a potential drug. This development exhibits that there could be a way to reach the problem area in the brain and stop the damage at its source.
The team believes that with proper human trials and safety checks, both the miRNA-based therapy and honokiol could go beyond just managing symptoms — they might actually cure Alzheimer’s, or at least stop it in its tracks.
And there’s more. Along the way, the researchers identified a full list of miRNAs that go up or down in Alzheimer’s brains. These could work like early warning signs, much like the red lights on a car dashboard — helping doctors detect the disease long before serious damage sets in.
If this approach works, it could lighten the heavy emotional and financial burden Alzheimer’s places on families and healthcare systems. More importantly, it could open up a new way of treating not just Alzheimer’s, but other brain diseases linked to inflammation and nerve cell damage.
(Edited by Muhammed Fazil.)
