New Alzheimer’s Treatment Strategy Reverses Cognitive Decline in Mice
Researchers have developed a new compound that could change the way we treat Alzheimer’s This disease offers not only a new weapon, but also a potentially new strategy in combating the most common form of dementia worldwide.
While current medications for Alzheimer’s mostly focus on eliminating amyloid-beta plaques The new compound takes a fundamentally different approach in relation to disease; instead, it targets a specific enzyme to therapeutically reprogram it. epigenome neurons – a set of molecular marks that can be added to or removed from DNA to change the way genes work.
monoclonal antibody Drugs that target amyloid-beta proteins, such as lecanemab and donanemab, help slow the progression of the disease somewhat when treatment is started early, but there is still no proven way to reverse cognitive decline from Alzheimer’s in humans.
Treatments that target another protein called tau Doesn’t seem very effectiveany.
It led researchers to suspect it might be us. I’m thinking about Alzheimer’s disease all wrong – Focusing on the proteins that are symptoms of the disease, rather than the root cause of the disease.
The new compound, called FLAV-27, appears to work more broadly; is moving away to target upstream changes in gene expression that help accelerate disease progression in many ways, not just through protein plaques.
This points to a new epigenetic strategy for the treatment of Alzheimer’s disease. says first author Aina Bellver-Sanchis is a molecular biologist at the Institute of Neurosciences at the University of Barcelona in Spain.
“The FLAV-27 compound represents an innovative and promising approach to Alzheimer’s disease.” says Bellver-Sanchis “has the potential to alter the disease process because it acts not only on symptoms or a single pathological biomarker, but also on the underlying molecular mechanisms.”
Bellver-Sanchis and colleagues Notes While monoclonal antibodies It represents a real breakthrough in Alzheimer’s treatment, lecanemab and donanemab it only slows cognitive decline by about 30 percent and only addresses some of the pathology of the condition.
Subscribe to ScienceAlert’s free, verified newsletter
FLAV-27 is the first inhibitor of its kind to target an enzyme called euchromatic histone-lysine N-methyltransferase 2 (EHMT2), also known as G9a.
G9a is involved in epigenetic regulation in the brain and can silence genes important for important tasks such as brain cell development, synaptic plasticity, and memory processing.
FLAV-27 inhibits G9a by blocking a molecule known as G9a. S-adenosylmethionineWithout this, the enzyme loses its effect on genetic expression, the researchers explain.
Blocking G9a appears to help calm epigenetic dysregulation seen in Alzheimer’s diseaseThey report and give brain cells a more typical function.
The new compound has not yet been tested in humans and may not be tested for some time, but it has shown promising results in studies on nematodes and mice, as well as in cell experiments.
Beyond reducing amyloid-beta plaques and mixed tau FLAV-27 in laboratory-grown mouse brain cells showed signs that it might help repair some of the damage caused by Alzheimer’s disease in another animal model. Caenorhabditis elegans.
In these nematode worms, the compound increased motility, extended lifespan, and accelerated mitochondrial respiration, which helps fuel cells.
FLAV-27 also restored memory performance, social behavior, and the function of signaling centers called synapses that connect brain cells in mouse models of both early- and late-onset Alzheimer’s.
Related: Promising New Drug Reverses Mental Decline in Mice with Advanced Alzheimer’s Disease
This reversal, researchers to recommendIt implies that epigenetic dysregulation is not just a side effect of the disease but may be a central mechanism linking various pathological markers of Alzheimer’s.
The team states that the new compound shows potential just like other drug candidates, but it still faces a long road before human trials can begin. notesIncluding toxicology studies in at least two animal species and other regulatory steps.
The study was published on: Molecular Therapy.
