Alzheimer's disease: Strategies for Disease Modification

Alzheimer's is a disease that needs serious attention because beside the fact that it harms and stresses the one who is diagnosed with it also affects their family as well; on top of this it is the largest unmet medical need in neurology. This disease doesn’t discriminate many of history leaders have battled this disease. Those such as former President Ronald Reagan and Civil Rights Leader Rosa Parks are just a couple but it has had it affects on more than five million Americans. Alzheimer’s and dementia goes hand in hand. Dementia is a loss of brain function that occurs with certain diseases. Alzheimer's disease (AD) is one form of dementia that gradually gets worse over time. It affects memory, thinking, and behavior. Memory impairment, as well as problems with language, decision-making ability, judgment, and personality, is necessary features for the diagnosis. Age and family history are risk factors for AD. As you get older, your risk of developing AD goes up. However, developing Alzheimer's disease is not a part of normal aging. Having a close blood relative, such as a brother, sister, or parent who developed AD increases your risk. Having certain combination of genes for proteins that appear to be abnormal in Alzheimer's disease also increases your risk. Other risk factors that are not as well proven include is longstanding high blood pressure. An article I found was Alzheimer's disease: Strategies for Disease Modification and basically this article explain how there are and have been attempts to modifying this terrible disease. It explains how current drugs improve symptoms, but do not have profound disease-modifying effects. However, in recent years, several approaches aimed at inhibiting disease progression have advanced to clinical trials. Among these, strategies targeting the production and clearance of the amyloid peptide; a cardinal feature of Alzheimer's disease that is thought to be important in disease pathogenesis are the most advanced. Approaches aimed at modulating the abnormal aggregation of tau filaments (another key feature of the disease), and those targeting metabolic dysfunction, are also being evaluated in the clinic. This article discusses recent progress with each of these strategies, with a focus on anti-amyloid strategies, highlighting the lessons learned and the challenges that remain.

Nature Reviews Drug Discovery 9, 387-398 (May 2010) | doi: 10.1038/nrd2896