Scientists tested the substance on rats with positive results and are now seeking partnerships with pharmaceutical companies to conduct clinical trials.
A research team at the Federal University of ABC (UFABC) in Brazil has created a new chemical compound that may help in the treatment of Alzheimer’s disease. Their investigation used computer modeling (in silico), laboratory cell studies (in vitro), and tests involving animals (in vivo), all of which produced encouraging early results. The researchers are now looking for pharmaceutical partners to move the compound into clinical testing.
Developed with support from FAPESP, the new compounds can be produced with relative ease and are thought to work by breaking down the beta-amyloid plaques that build up in the brains of individuals with Alzheimer’s disease. These plaques form when fragments of amyloid peptides collect between nerve cells, leading to inflammation and problems with neural signaling.
The study, published in ACS Chemical Neuroscience, explains that the compounds function as copper chelators. They attach to excess copper found within beta-amyloid plaques, helping to break them apart and lessen symptoms associated with the disease. In rat experiments, the compound improved memory, reduced issues with spatial orientation and learning, and produced biochemical changes consistent with the reversal of beta-amyloid plaque formation.
Copper Regulation as a Therapeutic Strategy
“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 [balance] has become one of the focuses for the treatment of Alzheimer’s,” explains Giselle Cerchiaro, a professor at the Center for Natural and Human Sciences at UFABC who coordinated the study.
Using this understanding, the team created a series of molecules capable of crossing the blood-brain barrier and extracting copper from beta-amyloid plaques. Out of the ten molecules produced for the project, three were chosen for trials in rats with induced Alzheimer’s disease. One of these candidates showed particularly strong results, demonstrating both effectiveness and safety.
The work was the subject of the doctoral thesis of FAPESP scholarship recipient Mariana L. M. Camargo, the master’s thesis of Giovana Bertazzo, and the undergraduate research project of Augusto Farias. A research group led by Kleber Thiago de Oliveira, a professor at the Federal University of São Carlos (UFSCar), helped with the research project by synthesizing one of the compounds studied.
In tests with rats, the compound reduced neuroinflammation and oxidative stress, as well as restored copper balance in the hippocampus, the region of the brain associated with memory. Animals treated with the substance also showed improved spatial orientation.
Reduction of Neuroinflammation and Restoration of Copper Balance
In addition to the behavioral results, the tests showed that the compound was non-toxic to hippocampal cell cultures or to the animals, the vital signs of which were monitored throughout the experiment. Computer simulations confirmed the compound’s ability to cross the blood-brain barrier and target the affected areas directly.
Alzheimer’s disease is a complex, multifactorial neurodegenerative condition for which there is still no cure or defined cause. Despite its high prevalence – an estimated 50 million people worldwide live with the disease – therapeutic options are limited and only offer symptom relief or consist of complex drugs, such as monoclonal antibodies.
The UFABC study has generated a patent application, and researchers are now seeking partnerships with companies to begin human clinical 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 celebrates.
Reference: “Novel Copper Chelators Enhance Spatial Memory and Biochemical Outcomes in Alzheimer’s Disease Model” by Mariana L. M. Camargo, Augusto B. Farias, Giovana B. Bertazzo, Rafael N. Gomes, Kaio S. Gomes, Lucas M. Bosquetti, Silvia H. Takada, Felipe C. Braga, Caroline C. Augusto, Bruno L. Batista, Kleber T. de Oliveira and Giselle Cerchiaro, 15 August 2025, ACS Chemical Neuroscience.
DOI: 10.1021/acschemneuro.5c00291
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1 Comment
“Alzheimer’s disease is a complex, multifactorial neurodegenerative condition for which there is still no cure or defined cause.” Correct! That’s why you can’t model Alzheimer’s in mice, who never develop human Alzheimer’s. In this study, the mice developed “Alzheimer’s” by injecting them with streptozotocin (STZ), a compound that kills pancreas cells and causes brain plaques. This is not Alzheimer’s disease. Some Alzheimer’s patients don’t have plaques, and some studies show plaques are protective of the brain against Alzheimer’s. And humans don’t get Alzheimer’s or brain plaques by injection of streptozotocin. Animal models of human disease are cruel and flawed, and lead to absurd comparisons. See my article, Of Mice and Men: The Problems Studying Mice to Learn about Men. https://www.academia.edu/127948044/Of_Mice_and_Men_The_Problems_with_Studying_Mice_to_Learn_about_Men