In a groundbreaking development, scientists have made a significant breakthrough in understanding the underlying causes of Alzheimer’s disease. For decades, Alzheimer’s has remained a perplexing mystery, but a recent study published in the journal Science has shed light on a previously elusive connection between abnormal proteins in the brain and a process known as necroptosis, a form of cellular suicide.
This discovery has been met with enthusiasm and excitement within the scientific community, as it opens new avenues for potential treatments. According to BBC News, Alzheimer’s disease is characterized by the gradual loss of neurons, the brain cells responsible for functions like memory. Upon examination of the brains of individuals with Alzheimer’s, researchers have consistently observed the accumulation of abnormal proteins called amyloid and tau.
However, until now, linking these key features of the disease has proven elusive. Researchers from the UK’s Dementia Research Institute at University College London and KU Leuven in Belgium propose a novel explanation. They suggest that abnormal amyloid begins to accumulate in the spaces between neurons, triggering brain inflammation—a condition neurons find unfavourable.
This inflammation sets in motion changes in the internal chemistry of neurons. Simultaneously, tangles of tau protein develop, and the affected brain cells start producing a specific molecule known as MEG3, which instigates cell death through necroptosis. Necroptosis is a normal mechanism our bodies use to eliminate unwanted cells as new ones are generated.
Crucially, the research team found that blocking the MEG3 molecule allowed brain cells to survive. This discovery represents a significant breakthrough in Alzheimer’s research, offering insights into the mechanisms behind neuron death. For decades, speculation abounded, but no one could pinpoint the precise mechanisms involved. Now, there is convincing evidence pointing to this specific cellular suicide pathway.
The breakthrough came through experiments involving the transplantation of human brain cells into genetically modified mice. These mice were engineered to produce copious quantities of abnormal amyloid. Recent progress has been made in developing drugs that can remove amyloid from the brain, marking the first treatments capable of slowing the destruction of brain cells.
Professor Bart De Strooper, a researcher at the UK’s Dementia Research Institute, suggests that the discovery of blocking the MEG3 molecule could open a new avenue of drug development. However, it’s important to note that extensive research will be required, spanning several years, before this potential treatment becomes a reality.
Professor Tara Spires-Jones, from the University of Edinburgh and the president of the British Neuroscience Association, praised the study, calling it a “cool paper” that addresses a fundamental gap in Alzheimer’s research. She emphasized the significance of these results for the field while also cautioning that many more steps need to be taken before this knowledge can be translated into an effective Alzheimer’s treatment.
Dr. Susan Kohlhaas, from Alzheimer’s Research UK, expressed excitement about the findings but acknowledged that they are still in the initial stages. She highlighted the importance of this discovery, as it unveils previously unknown mechanisms of cell death in Alzheimer’s disease, potentially paving the way for future treatments to slow or even halt the progression of the disease.
