NBS-nytt
11.06.2019
Alzheimer's disease (AD) has puzzled scientists for over a century. Years and years of work on AD has yet to produce a cure, and failing drug candidates have proven to be common. AD is the most common form of dementia and deprives affected individuals of a full life. In the end, individuals, families, and societies suffer from this burden. Here, we present a new piece for the AD puzzle.
Human lifespan is currently increasing. With new cases of AD increasing in parallel, large socio-economic challenges are becoming apparent and science has yet to produce a cure. Many attempts have been made to produce novel drugs to intervene with or reverse disease progression, but many have also failed during clinical trials. This problem is complicated by the lack of natural model organisms: natural analogues of the disease-causing proteins are hard to find.
The three common accepted pillars of AD aetiologies are neuroinflammation,amyloid (A) plaques and tau tangles; all these symptoms serve as potential targets for drug development. As A plaques seemed directly related to the severity of disease, it was thought that removal of A plaques could have therapeutic potential and so were targeted. Unfortunately, antibodies directed against these plaques disappointed in clinical trials, making them one of the many examples of how AD continues to hide its exact etiology. If these plaques are not the only problem, what else is there? Newer research has shown that defects in a process called mitophagy could be a new hallmark of the disease. A research group at UiO and Akershus University Hospital lead by Dr. Evandro
Gå til medietThe three common accepted pillars of AD aetiologies are neuroinflammation,amyloid (A) plaques and tau tangles; all these symptoms serve as potential targets for drug development. As A plaques seemed directly related to the severity of disease, it was thought that removal of A plaques could have therapeutic potential and so were targeted. Unfortunately, antibodies directed against these plaques disappointed in clinical trials, making them one of the many examples of how AD continues to hide its exact etiology. If these plaques are not the only problem, what else is there? Newer research has shown that defects in a process called mitophagy could be a new hallmark of the disease. A research group at UiO and Akershus University Hospital lead by Dr. Evandro