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Scientists at the Massachusetts Institute of Technology (MIT) have discovered a ‘remarkable’ new way to reverse Alzheimer’s.
It is approximated that more than six million Americans are currently living with Alzheimer's disease, which is the most common type of dementia. More than 55 million people have dementia worldwide and this number is expected to ‘almost double’ every 20 years, reaching 78 million in 2030 and 139 million in 2050, according to Alzheimer’s Disease International.
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Alzheimer's disease is a neurodegenerative disease that typically starts slow and progressively worsens over time. It affects the nervous system and breaks down communication around the body, eventually resulting in death.
Researchers at the MIT used a peptide, short chains of amino acids linked by peptide bonds, to disrupt CDK15, an enzyme that is usually overactive in the brains of people with Alzheimer’s disease.
When CDK15 is overactivated it harms neurons which leads to cognitive decline.
The researchers behind the study, which was published in the peer-reviewed journal, Proceedings of the National Academy of Sciences (PNAS), hope that their findings can serve as the focal point for future research into a drug to reverse the effects of Alzheimer’s disease.
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The study showed that when the peptide was tested on mice with Alzheimer’s disease who had an overactive CDK5, there was less DNA damage, neural inflammation and neuron loss.
These results were compared to a control group of mice given a scrambled version of the peptide.
Mice with Alzheimer’s who have a mutant Tau protein from, which leads to brain protein tangles, were also tested by researchers using the peptide.
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According to the non-profit organisation BrightFocus, tau proteins in the brains of people with Alzheimer’s disease are ‘misfolded and shaped’ in comparison to normal tau protein, which forms part of a structure called a microtubule.
Tau, which is mostly found in brain cells, has many functions. The microtubule's function is to help transport nutrients from one part of the nerve cell to another.
In mice who are genetically designed to lack tau protein, their brain cells do not function properly and tau dysfunction has been linked to a number of severe human brain diseases.
Researchers found that the mice in their recent peptide study had few Tau prevalence and neuron loss.
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There were also benefits identified regarding the behaviour of the mice. The mice who received the peptide were better at tasks, like navigating a water maze, than mice given the control peptide.
Li-Huei Tsai, the study’s senior author, said: “We found that the effect of this peptide is just remarkable. We saw wonderful effects in terms of reducing neurodegeneration and neuroinflammatory responses, and even rescuing behaviour deficits.”
Gregory Robinson