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.
AI 生成的图像

Brazilian copper-targeting compound reverses Alzheimer’s-like deficits in rats

AI 生成的图像
事实核查

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.

人们在说什么

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.

相关文章

Lab scene showing arginine supplements reducing Alzheimer’s pathology in mice and fruit flies, with healthy animals, brain scans, and positive research graphs.
AI 生成的图像

Arginine supplement curbs Alzheimer’s pathology in animal models

由 AI 报道 AI 生成的图像 事实核查

Researchers at Kindai University report that oral arginine, a common amino acid, suppresses amyloid‑β aggregation and its toxic effects in fruit fly and mouse models of Alzheimer’s disease. In treated animals, amyloid buildup fell, inflammation markers dropped, and behavioral performance improved, suggesting arginine could be a low‑cost candidate for drug repurposing.

Scientists at Northwestern University have identified a toxic subtype of amyloid beta oligomers that triggers early Alzheimer's changes in the brain. Their experimental drug, NU-9, reduced this damage and inflammation in pre-symptomatic mice, suggesting potential for preventing the disease before symptoms appear. The findings highlight a new strategy for early intervention.

由 AI 报道

Researchers have demonstrated that restoring levels of a key brain energy molecule can reverse advanced Alzheimer's disease in mouse models, repairing damage and restoring cognitive function. The study, published on December 22, challenges the long-held view that the condition is irreversible. Findings from human brain tissue support the approach's potential relevance to patients.

Researchers at Osaka Metropolitan University report that while the Alzheimer’s drug lecanemab reduces amyloid plaques, MRI measures found no improvement in the brain’s glymphatic waste-clearance three months after treatment began, underscoring the disease’s complexity and the need for multi-target approaches.

由 AI 报道

阿尔茨海默病试验正转向受癌症研究启发的多靶点方法,即便Novo Nordisk的司美格鲁肽试验失败。只有两种药物——Eli Lilly的Kisunla和Eisai与Biogen的Leqembi——被广泛批准用于减缓疾病进展。这种演变将这种脑部退化疾病视为复杂系统,在其全球影响下寻求新的遏止途径。

Scientists have created innovative nanoparticles designed to destroy harmful proteins linked to dementia and cancer. These particles can access difficult tissues like the brain and precisely eliminate problematic proteins without broad side effects. The technology shows early promise for precision medicine.

由 AI 报道 事实核查

Researchers at Case Western Reserve University report they have identified an abnormal interaction between the Parkinson’s-linked protein alpha-synuclein and the enzyme ClpP that disrupts mitochondrial function in experimental models. They also describe an experimental compound, CS2, designed to block that interaction, which they say improved movement and cognitive performance and reduced brain inflammation in lab and mouse studies.

 

 

 

此网站使用 cookie

我们使用 cookie 进行分析以改进我们的网站。阅读我们的 隐私政策 以获取更多信息。
拒绝