A new study from scientists at the UK Dementia Research Institute has found that human neurons are more vulnerable to Alzheimer’s disease than mouse neurons, a possible breakthrough for treatment. The study also identified a long noncoding RNA called MEG3 as a potential therapeutic target for the disease.
The scientists transplanted human brain cells into mice which they then manipulated.
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The study has important implications for the understanding and treatment of Alzheimer’s disease. The fact that human neurons are more vulnerable to the disease than mouse neurons suggests that there is a human-specific factor that contributes to the development of AD.
The identification of MEG3 as a potential therapeutic target is also very promising. MEG3 is a long noncoding RNA, which is a type of RNA that does not encode proteins. However, long noncoding RNAs can play important roles in regulating gene expression and other cellular processes.
The study found that MEG3 is upregulated in both AD patients and human neurons xenografted into the brains of AD mice. Additionally, MEG3 expression alone was sufficient to induce necroptosis, a type of programmed cell death, in human neurons in vitro.
Downregulation of MEG3 and inhibition of necroptosis rescued neuronal cell loss in xenografted human neurons. This suggests that MEG3 and necroptosis may play a role in the development and progression of AD.
The study also suggests that targeting MEG3 and necroptosis may be a promising therapeutic approach for AD. Further research is needed to validate these findings and to develop drugs that can safely and effectively target MEG3 and necroptosis in the brain.
Alzheimer’s disease is a progressive neurodegenerative disorder that gradually destroys memory and thinking skills, and eventually, the ability to carry out the simplest tasks. It is the most common cause of dementia in people over the age of 65.
Alzheimer’s disease is caused by the abnormal build-up of proteins in and around brain cells. These proteins form plaques and tangles that disrupt the communication between neurons and eventually lead to cell death.
The exact cause of Alzheimer’s disease is unknown. There is no cure for Alzheimer’s disease, but there are treatments that can help to manage the symptoms and slow the progression of the disease. These treatments include medications, lifestyle changes, and cognitive therapy.
“This is a very important and interesting finding,” researcher Prof Bart De Strooper, from the UK’s Dementia Research Institute, told the BBC. For the first time we get a clue to how and why neurons die in Alzheimer’s disease. There’s been a lot of speculation for 30-40 years, but nobody has been able to pinpoint the mechanisms.”
“It really provides strong evidence it’s this specific suicide pathway.”
The UK DRI is a landmark initiative. It unites seven centers to transform dementia discovery science, speeding up the global search for preventions, treatments and technologies that change lives.
“Alzheimer’s disease is a biological problem that can be solved by bringing together the right people and the right ideas,” said Bart De Strooper.
