A tale of transgenic mice: Heart failure medication might prevent, and reverse Alzheimer’s Disease How do we treat Alzheimer’s Disease (AD)? Almost every professional that has worked closely with dementia patients knows that AD is progressive and fatal. But what if it isn’t? What if there was a drug that could prevent or even treat it? As of today, AD is a progressive neurodegenerative disorder, the most common type of dementia that in advanced stages, causes severe memory and learning impairments as well as loss of motor function. One of the hallmarks of a brain affected by AD is the presence and accumulation of a sticky protein called beta-amyloid (Aβ), or Aβ plaques between nerve cells. This accumulation and deposition is thought to disrupt cell-to-cell communication and ultimately result in neuronal cell death and decreased brain volume. It is believed to be the primary driving force of AD pathogenesis. This idea, which is referred to as the “amyloid hypothesis,” has been the mainstream concept used to explain AD progression for the past two decades. Even then, it is crucial to note that not all researchers are convinced that beta-amyloid is the primary cause of Alzheimer’s, but most agree that it is a key component to understanding the disease.