Alzheimer's disease, the leading cause of dementia, affects over 55 million people worldwide. The disease is characterized by the buildup of amyloid-beta plaques and tau protein tangles in the brain, which disrupt cell communication and lead to the widespread death of nerve cells. The consequences of this massive cell loss are the heartbreaking cognitive decline and memory loss for which the condition is well known.
Despite extensive research, for decades the only treatments available for Alzheimer's offered temporary symptom management at best. Recently, however, the first drugs designed to target amyloid plaques have received (controversial) approval. While these new treatments successfully remove amyloid plaques, their clinical benefit in terms of improving cognition and memory has yet to be convincingly demonstrated.
A conundrum underscoring once more the need to prevent nerve cell death to stop the cognitive impairment that affects Alzheimer's patients. In a new study published in Science Translational Medicine , a team of researchers led by Prof. Dietmar Thal, Prof.
Bart De Strooper, and Dr. Sriram Balusu demonstrates they can indeed prevent loss of nerve cells in a mouse model of Alzheimer's using specific inhibitors. Necroptosis "Nerve cells die in the context of Alzheimer's disease as a consequence of a well-defined sequence of biochemical reactions, called 'necroptosis,'" explains Balusu, postdoctoral researcher in the lab of De Strooper at the VIB-KU Leuven Center .
