Monash University researchers have discovered that the compound Cu(ATSM), which supplies copper to the brain, may be effective in reducing toxic proteins associated with Alzheimer's, while improving memory in laboratory models.

The study, published in the journal ACS Chemical Neuroscience, reveals that Cu(ATSM) decreases levels of beta-amyloid in the brain, a protein linked to the disease, thus improving cognitive function.

Cu(ATSM) acts by increasing the activity of P-glycoprotein (P-gp) pumps, essential for clearing the brain of toxic substances. This effect restores elimination mechanisms, decreasing amyloid by 42% during the study.

Implications for future therapies

Since Cu(ATSM) has already been tested in other neurological conditions, it could quickly advance to human trials, offering new hope for the treatment of Alzheimer's symptoms.

Joseph Nicolazzo, director of the Center for Candidate Drug Optimization at the Monash Institute of Pharmaceutical Sciences and lead author of the study, said the compound has great potential as it has undergone safety evaluations for other diseases.

“Cu(ATSM) is a copper compound with anti-inflammatory and neuroprotective properties that has already advanced to the clinical trial phase for conditions such as Parkinson's and ALS,” Nicolazzo said.

While the results are encouraging, researchers continue to investigate how Cu(ATSM) affects amyloid clearance. There is particular interest in its effect on microglia activity, which may influence treatment efficacy.

For the treatment of Alzheimer's

Future studies will focus on exploring the mechanisms behind these findings.

Repairing the brain's elimination system could be key in the development of effective therapies in a context where the incidence of dementia is increasing.

Effectiveness compared to other treatments

Currently approved treatments for Alzheimer's are divided into two groups:

Traditional symptomatic treatments (the most used): include acetylcholinesterase inhibitors (such as donepezil, rivastigmine) and memantine. These only relieve symptoms without curing the disease or stopping its progression.

New anti-beta-amyloid monoclonal antibodies: lecanemab and donanemab, recently approved, which reduce beta-amyloid deposits in the brain, but are moderately effective in improving cognitive function and with risks of adverse effects.

Cu(ATSM) shows a different and potentially more promising mechanism of action in experiments: instead of just reducing beta-amyloid, it restores the brain's metabolic waste removal mechanisms, repairing P-glycoproteins at the blood-brain barrier.

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