Scientists successfully reverse Alzheimer’s in mice by removing ‘zombie cells’ fuel the disease – but they can’t work out how to do it in humans
- It’s not clear how ‘zombie cells’ originate but they are affect strokes, arthritis and heart attacks
- Mayo Clinic scientists reversed Alzheimer’s by editing them out of mice
- But they can’t do that in humans, and more research is needed to work out how to use this information to benefit humans
Alzheimer’s disease is caused by ‘zombie cells’ in the brain, according to new research.
Flushing out the lifeless cells could cure the devastating condition – as well as other neurological disorders, say scientists.
Known medically as senescent cells, they lose their capacity to divide – accumulating throughout the body with age.
They have been dubbed ‘zombies’ because they can’t die – but are equally unable to perform the functions of a normal cell.
In experiments on mice engineered to develop a rodent form of dementia the US team found they gather in neurons prior to mental decline.
It’s not clear how ‘zombie cells’ originate but they are affect strokes, arthritis and heart attacks. Mayo Clinic scientists reversed Alzheimer’s by editing them out of mice. But they can’t do that in humans
Preventing this stopped the build up of a toxic protein, called tau – a hallmark of Alzheimer’s – leading to the retention of brain cells and memory.
Senior author Dr Darren Baker, a molecular biologist at the Mayo Clinic in the United States, said senescent cells have been linked to a host of illnesses including arthritis, strokes and heart attacks.
He said: ‘Senescent cells are known to accumulate with advancing natural age and at sites related to diseases of ageing including osteoarthritis, atherosclerosis and neurodegenerative diseases such as Alzheimer’s and Parkinson’s.
‘In prior studies we have found that elimination of senescent cells from naturally aged mice extends their healthy life span.’
Cellular senescence helps keep humans predominantly free of cancer in the first half of life.
But as we age the senescent cells accumulate – secreting inflammatory molecules that can damage neighbouring tissue and help trigger several diseases of ageing.
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In the study, published in the journal Nature, the research team used a mouse model that imitates Alzheimer’s.
First author Tyler Bussian, a student in Dr Baker’s lab, said: ‘We used a mouse model that produces sticky, cobweb like tangles of tau protein in neurons and has genetic modifications to allow for senescent cell elimination.
‘When senescent cells were removed we found the diseased animals retained the ability to form memories, eliminated signs of inflammation, did not develop neurofibrillary tangles and had maintained normal brain mass.’
Using a drug that removed the zombie-like cells also helped stop the tau proteins clumping together – a process that destroys brain cells.
Dr Baker said his team was also able to identify the specific type of cell that became senescent in regions of the brain such as the hippocampus – that controls memory.
Mr Bussian said: ‘Two different brain cell types called ‘microglia’ and ‘astrocytes’ were found to be senescent when we looked at brain tissue under the microscope.
‘These cells are important supporters of neuronal health and signalling so it makes sense senescence in either would negatively impact neuron health.’
Dr Baker said the finding was somewhat surprising since a causal link between senescent cells and neurodegenerative disease had not been established.
He said: ‘We had no idea whether senescent cells actively contributed to disease pathology in the brain.
‘To find it’s the astrocytes and microglia that are prone to senescence is somewhat of a surprise as well.’
Dr Baker said the research lays out the best-case scenario where prevention of damage to the brain prevented disease.
It could open up a potential new therapeutic avenue for the treatment of neurodegenerative diseases.
In the mice his team removed these cells using genetic modification throughout the lifespan.
Continuous clearance prior to the onset of neurodegenerative disease may have a significant effect on disease progression.
Further research will be required to determine whether this translates to humans and could be used in a clinical setting.
Dr Baker added: ‘Clearly, this same approach cannot be applied clinically, so we are starting to treat animals after disease establishment and working on new models to examine the specific molecular alterations that occur in the affected cells.’
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