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Alzheimer’s breakthroughs offer new promise for reversing and preventing brain decline

Alzheimer’s breakthroughs offer new promise for reversing and preventing brain decline
Alzheimer’s breakthroughs offer new promise for reversing and preventing brain decline | Photo: Steven HWG

Recent scientific advances published in December 2025 have injected new optimism into the global fight against Alzheimer’s disease, suggesting that one of the most devastating neurological disorders may one day be reversible or even preventable.


Two separate studies — one focused on restoring the brain’s cellular energy supply and another on blocking the earliest toxic protein species — mark a significant leap forward in understanding how to stop cognitive decline before it begins.


Alzheimer’s currently affects more than 55 million people worldwide, a number expected to rise sharply with ageing populations. The condition remains a leading cause of disability in older adults, making progress toward effective treatment a matter of global health and sustainability. These findings, while still limited to animal models, point to a potential shift from late-stage management to prevention and regeneration.


Restoring the brain’s energy balance through NAD+ stabilisation

A study released on 22 December 2025 in Cell Reports Medicine identified that a dramatic drop in nicotinamide adenine dinucleotide (NAD+), an essential molecule for cellular energy production, may be a central driver of Alzheimer’s progression. Using an experimental compound called P7C3-A20, researchers successfully stabilised NAD+ levels in mice with advanced Alzheimer’s, restoring normal brain metabolism.


The results were striking. Treated mice not only showed repaired brain tissue and normalised biomarkers such as phosphorylated tau 217 but also demonstrated a full recovery of memory and cognitive performance. However, the study’s authors cautioned against using over-the-counter NAD+ boosters, warning that excessive levels could pose cancer risks. P7C3-A20 instead maintains NAD+ within a healthy physiological range, providing a safer and more balanced approach.


The research underscores how energy regulation and metabolic resilience may be just as important to brain health as the removal of toxic proteins — a growing area of focus in age-related neuroscience.


NU-9 shows preventive potential by targeting toxic amyloid subspecies

Meanwhile, a separate study from Northwestern University in December 2025 examined a compound called NU-9, originally developed for amyotrophic lateral sclerosis (ALS).


Researchers discovered that NU-9 neutralises a highly toxic, previously unknown subspecies of amyloid beta oligomers (designated ACU193+) that triggers inflammation and neuronal damage early in Alzheimer’s development.


In pre-symptomatic mice, a 60-day oral course of NU-9 sharply reduced early inflammation, known as reactive astrogliosis, and lowered the buildup of harmful proteins. Scientists compared its potential role to cholesterol-lowering statins — medications taken before symptoms arise to prevent disease onset. With NU-9 already cleared for initial human trials in ALS, researchers hope this drug could one day form the foundation of pre-symptomatic Alzheimer’s prevention.


A wider scientific momentum across 2025

These developments come amid a broader surge of progress. Studies published throughout 2025 reported other promising directions: targeted lithium compounds capable of restoring youthful brain activity, cancer drugs like letrozole and irinotecan reversing harmful gene expression patterns, and bioactive nanoparticles repairing the blood-brain barrier to enhance waste clearance and cognitive recovery.


Together, these breakthroughs illustrate that Alzheimer’s is not a single disease process but a convergence of metabolic, inflammatory, and genetic failures — requiring multifaceted therapies rather than one cure-all.


A cautious optimism for the future

Although human trials are still forthcoming, 2025 marked a turning point in Alzheimer’s research. The concept of reversing existing damage or preventing it altogether is no longer distant speculation. It reflects a scientific shift toward understanding the disease’s earliest molecular mechanisms — and designing interventions that promote long-term brain resilience.


Sustained international collaboration, open-access data, and investment in early diagnostics remain crucial to turning these laboratory successes into real-world therapies. Readers can explore current studies and ongoing trials through institutions such as Cell Reports Medicine and Northwestern University’s Alzheimer’s Research Center, which continue to publish updates on this fast-moving field.


If confirmed in humans, these discoveries could redefine ageing itself — offering millions a future in which memory loss is no longer inevitable but instead preventable and, perhaps, reversible.

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