Australian Study Finds New Treatment for Alzheimer’s Patients
There are new medical developments in the diagnosing and treating of chronic conditions like diabetes, heart disease, and cancer. This is leading to people living longer and healthier lives. But there are some drawbacks too.
Some conditions like Alzheimer’s and other forms of dementia have been growing in number as populations age, according to a press release from Monash University in Australia. With people living longer, finding a treatment that can halt cognitive decline became crucial. Researchers at the university studied a potential treatment using a drug which delivers copper to the brain to reduce toxic-proteins called amyloid-beta. The hope was that this would lead to improved cognition and memory in Alzheimer’s patients.
About the Research
The study published in June in the journal ACS Chemical Neuroscience showed that the copper-based compound Cu(ATSM) – copper compound – repairs a waste-clearing pump at the blood-brain barrier, reported Melbourne Insider.
When the waste clearing pump is operating correctly, the proteins are expelled from the brain. When it is not functioning correctly, as is the case with Alzheimer’s patients, the amyloid-beta stays in the brain and causes cognitive decline. Over the course of 56 days, the Cu(ATSM) reduced amyloid-beta levels by 42 percent. The patients’ memory also improved.
“This is the first study to show that Cu(ATSM) can increase the abundance of P-gp clearance pumps in an Alzheimer’s model, effectively linking the repair of the blood-brain barrier to a reduction in toxic proteins and improved cognitive function,” Dr Jae Pyun, the lead author from the drug delivery, disposition and dynamics department at Monash Institute of Pharmaceutical Sciences (MIPS), said in the press release from Monash University.
What’s Next?
The Cu(ATSM) compound has anti-inflammatory and neuroprotective properties and has been used in clinical trials for other neurological diseases like Parkinson’s and ALS, according to the press release.
“Because reducing amyloid burden is clinically proven to improve functional outcomes, these preclinical results strongly support the rationale for testing this drug in early symptomatic Alzheimer’s disease,” said Senior author Professor Joseph Nicolazzo, the director of the Centre for Drug Candidate Optimization at MIPS.
The researchers are still looking at the way the compound works in the body. Besides repairing the blood-brain barrier, it may also allow the brain’s immune cells to consume the plaque. Future studies will focus on how the toxic proteins exit the brain and the role of the brain’s immune cells. This offers hope that cognitive dysfunction and memory loss could be halted and even restored in people with Alzheimer’s.
