Alzheimer’s disease (AD), characterized by an accumulation of β-amyloid protein (Aβ) in brain tissue, is a leading cause of dementia. Researchers at Tokyo University of Science have previously reported on the oxytocin-induced reversal of impaired synaptic plasticity triggered by amyloid β peptide (25-35) (Aβ25-35). They now show that an oxytocin derivative with modifications to enhance brain perfusion can reverse Aβ25-35-induced cognitive impairment in mice.
The cognitive decline and memory loss observed in Alzheimer’s disease (AD) is attributed to the accumulation of β-amyloid protein (Aβ), which impairs neural function in the brain. Experimentation has shown that oxytocin, a peptide hormone primarily responsible for parturition, bonding, and lactation, also regulates cognitive behavior in the rodent central nervous system (CNS). This finding, along with the identification of…
