Illustration of a Brazilian researcher in a lab examining a rat, with screens showing brain scans and molecular structures, representing a new compound that reverses Alzheimer's-like deficits in rats.
Illustration of a Brazilian researcher in a lab examining a rat, with screens showing brain scans and molecular structures, representing a new compound that reverses Alzheimer's-like deficits in rats.
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Brazilian copper-targeting compound reverses Alzheimer’s-like deficits in rats

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Researchers at Brazil’s Federal University of ABC report a simple copper-chelating molecule that reduced beta-amyloid–linked pathology and improved memory in rats. The compound showed no detectable toxicity in preclinical tests and, based on computer modeling, is predicted to cross the blood–brain barrier. The team is seeking industry partners for clinical development.

A research team led by Giselle Cerchiaro at the Federal University of ABC (UFABC), Brazil, has developed a new copper-targeting compound that improved cognition and reduced disease markers in a rat model of Alzheimer’s disease. The work, supported by the São Paulo Research Foundation (FAPESP), is detailed in ACS Chemical Neuroscience (published August 15, 2025; DOI: 10.1021/acschemneuro.5c00291).

According to the paper and accompanying FAPESP release, the compounds act as copper chelators, binding excess copper associated with beta‑amyloid plaques and promoting their degradation. “About a decade ago, international studies began to point to the influence of copper ions as an aggregator of beta-amyloid plaques. It was discovered that genetic mutations and changes in enzymes that act in the transport of copper in cells could lead to the accumulation of the element in the brain, favoring the aggregation of these plaques. Thus, the regulation of copper homeostasis has become one of the focuses for the treatment of Alzheimer’s,” Cerchiaro said.

From an initial set of ten candidate molecules, three advanced to animal testing. In rats with an induced Alzheimer’s-like condition, one compound (identified in the study as L10) stood out: treated animals showed better performance on spatial memory tasks, along with reduced neuroinflammation and oxidative stress and a restoration of copper balance in the hippocampus. The study also reports a reversal in beta‑amyloid plaque patterns.

Safety assessments found no detectable toxicity in hippocampal cell cultures or in the treated rats at the tested doses; vital signs were monitored during experiments. In silico analyses predicted that the compound can cross the blood–brain barrier, supporting its potential as a drug candidate.

The project formed part of the doctoral thesis of Mariana L. M. Camargo, the master’s thesis of Giovana B. Bertazzo, and the undergraduate research of Augusto B. Farias. A team led by Kleber Thiago de Oliveira at the Federal University of São Carlos (UFSCar) synthesized one of the compounds. The findings have led to a patent application, and the researchers are pursuing partnerships to begin human trials. “It’s an extremely simple, safe, and effective molecule. The compound we’ve developed is much less expensive than available drugs. Therefore, even if it only works for part of the population, since Alzheimer’s disease has multiple causes, it’d represent a huge advance over current options,” Cerchiaro said.

Alzheimer’s affects an estimated 50 million people worldwide, and current treatments remain limited. If future studies confirm safety and efficacy in humans, a low‑cost, copper‑targeting approach could expand therapeutic options.

Was die Leute sagen

Initial reactions on X to the Brazilian copper-chelating compound for Alzheimer's are positive and limited, focusing on its potential to reverse symptoms in rats without toxicity. Users, including scientists and caregivers, shared the news highlighting memory restoration and calls for human trials. No significant negative or skeptical opinions were found in recent posts.

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Researchers at Sweden’s Karolinska Institutet and Japan’s RIKEN Center for Brain Science report that two somatostatin receptors, SST1 and SST4, jointly regulate levels of neprilysin—an enzyme that breaks down amyloid-beta—in the hippocampus. In mouse models, activating the receptors raised neprilysin, reduced amyloid-beta buildup and improved memory-related behavior, the team said.

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Alzheimer's trials are shifting to a multi-target approach inspired by cancer research, even after failures with Novo Nordisk's semaglutide. Only two drugs, Eli Lilly's Kisunla and Eisai and Biogen's Leqembi, are widely approved to slow progression. This evolution treats the brain-wasting disease as a complex system, seeking new ways to halt it amid its global impact.

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Rice University scientists say they have created the first complete, label-free molecular atlas of an Alzheimer’s brain in an animal model, combining hyperspectral Raman imaging with machine learning to map chemical changes that appear unevenly across brain regions and extend beyond amyloid plaques.

 

 

 

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