New Delhi: As much as Alzheimer’s is about losing memories, the neurodegenerative disorder also physically damages the brain and shrinks it over time.
For decades, researchers have known that Alzheimer’s is linked to the build-up of toxic proteins in the brain. But exactly how those proteins lead to brain damage was unclear. Scientists have finally identified the process which explains how Alzheimer’s and dementia kill off brain cells.
A study has now found that when toxic proteins accumulate inside a cell, they set off a series of chemical reactions, known as karyoptosis, where the cell’s nucleus and its genetic material shrivels before eventually breaking down completely.
The study, conducted by researchers from King’s College London and the UK Dementia Research Institute, was published on 25 June in the journal Nature Communications. It was based on an analysis of 3,000 brain cells collected from 28 people with either end-stage Alzheimer’s or frontotemporal dementia.
“The death and loss of cells in the brain drives many symptoms experienced by people living with dementia. Our study uncovers a new series of chemical events which can coordinate cell death in brain cells. We have started to lay out the road map of how karyoptosis works, and I’m excited to see future breakthroughs this may drive in the dementia research community and beyond,” Rebecca Casterton, senior researcher at the UK Dementia Research Institute at King’s and first author on the paper told ScienceDaily.
The team conducted experiments using rat neurons, human neurons, fruit flies, and mathematical models to see if blocking the process of karyoptosis could reduce cell death. They realised that interventions during the interaction between certain proteins (the kinase p38 MAP kinase and the protein LaminB1) could slow down or even prevent the breakdown of the nucleus.
“The identification of karyoptosis is a crucial step towards finding targets for treatments that could stop or slow cell loss. It could help widen the window for therapies that tackle the underlying causes of disease, bringing us closer to a cure for dementia,” Sara Rodrigues, Senior Research Manager at Alzheimer’s Research UK, told ScienceDaily.
The researchers highlighted that the next step in their study is to develop ways to target interactions between the proteins p38 MAP kinase and LaminB1 in humans to slow down cell death. This would also allow researchers to find other treatments for neurodegenerative diseases. However, it is important to note that such findings are still at a laboratory-stage and would require much more research before they turn into treatments for patients.