Researchers from the United Kingdom and Belgium believe they have unraveled the mystery of how brain cells perish in Alzheimer's disease, a question that has baffled scientists for years. Their findings, published in the journal Science, link the accumulation of abnormal proteins in the brain with a process known as "necroptosis," a form of cellular self-destruction. This discovery has generated excitement in the scientific community as it offers fresh insights into potential Alzheimer's treatments.
The primary manifestation of Alzheimer's disease is the loss of neurons (brain cells), leading to symptoms like memory loss. In the brains of individuals with Alzheimer's, there is a noticeable buildup of abnormal proteins called amyloid and tau. However, connecting these hallmark features of the disease has been a longstanding challenge.
The researchers, hailing from the Dementia Research Institute at University College London in the UK and KU Leuven in Belgium, propose a novel explanation. They suggest that abnormal amyloid accumulates in the gaps between neurons, triggering brain inflammation, which is detrimental to the neurons. This, in turn, alters the neurons' internal chemistry. The result is the formation of tau tangles and the production of a specific molecule called MEG3, which initiates cell death through necroptosis—a natural process used by the body to eliminate unwanted cells as new ones are generated. Blocking MEG3 allowed the brain cells to survive.
Researcher Prof Bart De Strooper, from the Dementia Research Institute in the UK, called this discovery significant and intriguing, marking the first time researchers have identified a possible mechanism for neuronal death in Alzheimer's. He emphasized that it provides strong evidence for this specific suicide pathway.
The breakthrough stemmed from experiments in which human brain cells were transplanted into genetically modified mice's brains programmed to produce abnormal amyloid in abundance. Recent advancements in drugs that remove amyloid from the brain have shown promise as the first treatments to slow the destruction of brain cells.
Prof De Strooper anticipates that blocking the MEG3 molecule to prevent brain cell death could open up a new avenue for drug development. However, he cautioned that extensive research is required before this becomes a reality.
Prof Tara Spires-Jones, the president of the British Neuroscience Association, praised the study for addressing a fundamental gap in Alzheimer's research and described the results as fascinating, yet she stressed the need for many more steps before determining its suitability as an Alzheimer's treatment.
Dr. Susan Kohlhaas, from Alzheimer's Research UK, deemed the findings exciting but emphasized that they are still in the early stages. This discovery is significant as it sheds light on previously unknown mechanisms of cell death in Alzheimer's, offering potential avenues for future treatments to slow or halt the disease's progression.
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