A drug that delivers copper to the brain could significantly reduce buildup of toxic proteins associated with Alzheimer's disease and improve long-term spatial memory, according to a study. Alzheimer's disease, a neurodegenerative condition with a progressive loss of speech, memory and thoughts, is driven by a buildup of toxic proteins called amyloid-beta. Researchers, including those from Australia's Monash University, said that normally, the brain flushes out the toxic proteins into the bloodstream through pumps in the blood-brain barrier.
However, in Alzheimer's disease, the pumps doing the heavy lifting -- called P-glycoprotein (P-gp) -- weaken significantly, clogging the drain and trapping the toxic proteins in the brain. Findings published in the American Chemical Society (ACS) Chemical Neuroscience show that a copper-containing compound 'Cu(ATSM)' repairs a vital waste-clearing pump in a mouse model with Alzheimer's disease, potentially unlocking a new avenue of therapeutics targeting neurovascular dysfunction.
Studies have shown that problems with the brain's waste clearance could increase one's risk of dementia, of which Alzheimer's disease is the most common form. Lead author Jae Pyun, from the drug delivery, disposition and dynamics theme at Monash Institute of Pharmaceutical Sciences (MIPS), said the treatment successfully engages the brain's blood vessels to lower toxic protein levels, resulting in behavioural benefits.
Pyun said the study is the first to show that the copper-containing compound can increase the abundance of P-gp clearance pumps in an Alzheimer's model, by 24.1 per cent, effectively linking the repair of the blood-brain barrier to a reduction in toxic proteins and improved cognitive function.
"By improving the pumps, the brain can finally clear out the trapped waste. Over 56 days, the treatment reduced toxic amyloid-beta by 42 per cent and improved spatial learning by nearly 44 per cent," Pyun said.
The authors wrote, "Cu(ATSM) (30 milligrams per kilogram per day for 56 days) restored brain microvascular P-gp abundance (24.1 per cent) and Cu concentrations (229.8 per cent) as well as significantly reduced brain cortical concentrations of human (amyloid protein) (42.1 per cent) in (diseased) mice." "Importantly, Cu(ATSM) treatment led to significantly improved (43.8 per cent) learning and long-term spatial memory in (diseased) mice," they said.
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