- While scientists still do not know what exactly causes Alzheimer’s disease, previous research shows there are a number of potential factors.
- A new study explains how a research team was able to use a new nanotechnology strategy to reverse Alzheimer’s disease in mice with the condition.
- The new nanotechnology helped reduce amyloid-beta in the mice’s brains by 50-60%.
Researchers continue to look for new ways of treating and possibly even reversing Alzheimer’s disease — a type of dementia affecting an estimated 55 million people worldwide as of 2020.
While scientists still do not know what exactly causes Alzheimer’s disease, previous research shows there are a number of potential factors including genetics,
“Alzheimer’s is growing fast with aging populations, and
“The disease also isn’t driven by a single mechanism with vascular dysfunction, inflammation, and
Battaglia is the lead author of a new study recently published in
For this study, researchers used nanoparticles, which Battaglia explained are like tiny programmable “shuttles.”
“They’re made from biocompatible materials and decorated with multiple tags that bind to specific receptors on the
“Once inside the
Battaglia said for this study, they decided to focus on the brain’s vasculature — or its blood system — rather than neurons or other brain cells because the vasculature, and especially the blood-brain barrier, sets the rules for what enters and leaves the brain.
“In Alzheimer’s, this gatekeeping and the brain’s clearance systems are compromised early. By restoring transport and clearance at the vascular interface, we can lower (the) toxic burden for all brain cells at once. It’s a unifying lever: if you fix the ‘plumbing,’ neurons and
glia are less stressed and can function more normally.”
— Giuseppe Battaglia, PhD
At the study’s conclusion, researchers found that one hour after mice mimicking Alzheimer’s disease were given three doses of their new nanotechnology — which they refer to as a “supramolecular drug” — the mice experienced a reduction of amyloid-beta in their brains between 50-60%.
“Speed matters,” Battaglia said. “A rapid drop shows we’re engaging the intended clearance pathway, not just altering a lab marker. It’s strong proof-of-mechanism that the nanoparticles cross the barrier, activate removal, and do so using the body’s own routes. While it’s an animal study, the pharmacodynamic profile, fast in, fast effect, is exactly what we want before moving toward clinical testing.”
Additionally, scientists observed a mouse aged equivalent to 60 human years recover the behavior of a healthy mouse six months after treatment when aged equivalent to 90 human years.
“It suggests the benefits are durable and functional, not only biochemical. Restoring vascular transport can translate into improved cognition-related behaviors over time, implying we’re improving brain resilience, not just clearing amyloid transiently. It’s still early and in mice, but long-lasting functional recovery is the kind of signal that justifies advancing toward human studies.”
— Giuseppe Battaglia, PhD
“We’re completing safety, dosing, and pharmacology studies in larger animal models, optimizing manufacturing to clinical-grade standards, and preparing regulatory packages for first-in-human trials,” Battaglia responded when asked about the next steps for this research.
“In parallel, we’re exploring combinations with existing therapies and testing whether the same vascular-targeted approach can help in other neurodegenerative conditions,” he said.
MNT spoke with Peter Gliebus, MD, chief of neurology and director of cognitive and behavioral neurology at Marcus Neuroscience Institute, a part of Baptist Health South Florida, about this study who commented he found it to be an interesting and exciting preliminary finding.
“It demonstrates that the blood-brain barrier plays a significant role in the development of Alzheimer’s disease. Enhancing the brain’s clearance mechanisms may lead to meaningful therapeutic strategies. Additionally, this supports the understanding that toxic amyloid accumulation is detrimental to brain function.”
— Peter Gliebus, MD
“It is very important for researchers to continue exploring different mechanisms, as having multiple approaches to influence disease progression could lead to better outcomes for patients,” he continued. “This multidimensional strategy may enhance the effectiveness of future treatments and provide better insights into the pathology of Alzheimer’s disease. The next steps would be translating this trial to humans.”
MNT also spoke with Clifford Segil, DO, neurologist at Providence Saint John’s Health Center in Santa Monica, CA, about this research.
“I am disappointed to see more research being aimed at decreasing early brain amyloid and tau proteins, as current late brain amyloid and tau medications are not producing any noticeable clinically noticeable improvement in memory loss in people,” Segil commented.
“Current medications are extremely effective at reducing brain amyloid and tau but post-marketing surveillance is not showing any noticeable improvements in memory unlike current weight loss medications whose use is noticeable almost immediately,” he added.
“It is important for researchers to continue to find new ways of treating memory loss in elderly patients with Alzheimer’s dementia because our mainstay oral therapies, which affect
Health">brain acetylcholine andHealth">NMDA , in addition to our new infusion and subcutaneous delivered anti-amyloid therapeutics, are limited in their ability to improve cognition and memory in patients with memory loss from a dementia.”
— Clifford Segil, DO
