the two proteins that are seen to cause issues in alzheimer’s disease are beta-amyloid and tau. beta-amyloid plaques build up between nerve cells, and twisted tau fibres end up inside the nerve cells. this double-edged sword of damage that hits nerve cells from both the outside and the inside leads to the symptoms of alzheimer’s disease, such as memory loss, cognitive decline and confusion, behaviour and mood changes, and difficulties with thoughts, language, and daily tasks.
in the early stages, when these proteins begin to accumulate in the brain, levels of glutamate, a neurotransmitter, are often much higher than they should be. this leads to damaging overactivity between nerve cells, a physiological process known as excitotoxicity, which causes cell death.
the troriluzole study
to perform the study, researchers from auburn university, led by drs. miranda reed and michael gramlich, genetically modified mice so that they could replicate the same signs and symptoms of the early stages of alzheimer’s disease.
the mice in question were shown to experience excitotoxicity caused by excessive glutamate in the brain, the same as in humans who develop alzheimer’s disease. because of the excessive glutamate, the animals replicated the signs and symptoms found in the early stages of alzheimer’s disease.