Much of the focus in Alzheimer's research remains on amyloid beta and the processes by which it accumulates in the brain. This researcher is one of a number of attempts over the years to produce a drug candidate that interferes beneficially in these mechanisms:
A molecular compound [restored] learning, memory and appropriate behavior in a mouse model of Alzheimer's disease. The molecule also reduced inflammation in the part of the brain responsible for learning and memory. [This] is the second mouse study that supports the potential therapeutic value of an antisense compound in treating Alzheimer's disease in humans. "Our current findings suggest that the compound, which is called antisense oligonucleotide (OL-1), is a potential treatment for Alzheimer's disease."
OL-1 blocks the overexpression of a substance called amyloid beta protein precursor, which normalized the amount of amyloid beta protein in the body. Excess amyloid beta protein is believed to be partially responsible for the formation of plaque in the brain of patients who have Alzheimer's disease.
Scientists tested OL-1 in a type of mouse that overexpresses a mutant form of the human amyloid beta precursor gene. Like people who have Alzheimer's disease, [the] mice have age-related impairments in learning and memory, elevated levels of amyloid beta protein that stay in the brain and increased inflammation and oxidative damage to the hippocampus - the part of the brain responsible for learning and memory.
Scientists found that learning and memory improved in the genetically engineered mice that received OL-1 compared to the genetically engineered mice that received random antisense. They also tested the effect of administering the drug through the central nervous system, so it crossed the blood brain barrier to enter the brain directly, and of giving it through a vein in the tail, so it circulated through the bloodstream in the body. They found where the drug was injected had little effect on learning and memory.