An international study in which Amaia Arranz, Ikerbasque researcher at the Basque Achucarro centre, has participated, shows a mechanism of neuronal death in Alzheimer’s disease, which may open the door to new therapies or drugs.
The study has been published in the prestigious journal Science.
Alzheimer’s disease remains an enigma to the scientific community, but a recent study published in the prestigious journal Science is shedding new light on the underlying mechanisms behind this devastating disease. This study follows research previously published in 2017 by the same group of researchers, and addresses the crucial question of how neurons die in this disease.
To address this question, the research team, in which Amaia Arranz, an Ikerbasque researcher at the Achucarro Neuroscience Centre, participated, transplanted human and mouse neurons into the brain of a mouse model of Alzheimer’s disease. The results were surprising: only the human neurons showed markers of the disease, such as Tau phosphorylation, neurofibrillary tangles and, most importantly, cell death. They also found that the human neurons in this model showed strong expression of MEG3, a long non-coding RNA that is also found at elevated levels in Alzheimer’s patients. This high expression of MEG3 appears to be related to cell death in these human neurons. More specifically, MEG3 appears to induce a type of cell death called “necroptosis” in these human neurons, leading to the loss of these cells.
The identification of MEG3 and its role in the necroptosis of human neurons provides a deeper understanding of the mechanisms underlying Alzheimer’s disease and makes MEG3 an important target for future research and therapies aimed at preventing neuronal death in Alzheimer’s patients. This is a finding of great importance, as neuronal death is a major feature of Alzheimer’s disease, leading to cognitive deficits and dementia in patients.
A thorough understanding of the mechanisms underlying this neuronal death is essential in the search for effective treatments and therapeutic targets, and given that there are currently no drugs that effectively cure or alleviate the symptoms of the disease, these findings open the door to the possibility of developing therapies that prevent the loss of neuronal cells, which could delay or even prevent the progression of the disease.
In the words of researcher Amaia Arranz: “Our findings are promising and open up new perspectives in Alzheimer’s disease research. By identifying a specific neuronal death mechanism in human neurons and proposing a possible treatment, we are taking an important step towards finding effective therapies for this disease.