Scientists discover new key to halting brain damage in Alzheimer’s
Scientists continue to learn more about the causes of Alzheimer’s disease, with each new discovery opening up more potential for prevention and treatment. At SuperAging News, we strive to keep you informed, and we’ve reported here, here and here on some of the most important new findings. Now a Flemish research team has discovered, in mice, a protective pathway against Alzheimer’s.
As reported here, “the findings open up new research avenues in the search for therapies that could halt or prevent the accumulation of brain damage occurring in Alzheimer’s.”
Alzheimer’s 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.”
Until now, treatments have been limited to management of symptoms. Now the first drugs to target amyloid plaques have been been approved. While they are somewhat successful in removing amyloid plaques, the clinical evidence that this leads to cognitive improvement is still inconclusive. To quote the article, this leaves us with “a conundrum underscoring once more the need to prevent nerve cell death to stop the cognitive impairment that affects Alzheimer’s patients.”
How can this be accomplished? The research team, led by Professor Dietmar Thal, Professor Bart De Strooper and Dr. Sriram Balusu succeeded in preventing loss of nerve cells in a mouse model of Alzheimer’s, using specific inhibitors.
The article quotes Dr. Balusu, a postdoctoral researcher at the VIB-KU Leuven Center for Brain & Disease Research: “Nerve cells die in the context of Alzheimer’s disease as a consequence of a well-defined sequence of biochemical reactions, called ‘necroptosis.” Last year, the team mapped the triggers for this necroptosis in human nerve cells transplanted into Alzheimer’s-affected mouse brains.
They further studied the role of necroptosis in different mouse models for Alzheimer’s, and found it was activated in mouse models with tau tangles but not in models that only exhibited amyloid plaques. The article quotes Professor Thal: “Our results suggest that there exists a disease-related, delayed from of nectroptosis that is activated by a specific form of tau.” They also found specific inhibitors that intercept the activation of necroptosis, preventing nerve cell loss and also improving the social recognition memory of the mice.
This suggests that necroptosis inhibition could be a promising new research pathway. Professor De Strooper says, “Our findings indicate that necroptosis inhibition should be investigated further as a potential therapeutic strategy that could complement current amyloid and tau-directed therapies for treating Alzheimer’s disease.”
We’ll keep our eyes on this emerging topic and bring you any new developments.
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