Health
Man resisting early-onset Alzheimer’s disease may hold clues to treatment
A mutation in DNA that causes a brain disease.
Men with a gene mutation known to cause early-onset Alzheimer’s disease delayed the onset of dementia until age 72. His story may inspire researchers developing drugs to treat Alzheimer’s and other ailments.
The patient, who is part of a large Colombian family with hereditary Alzheimer’s disease, asked a collaborative research team, including researchers from the University of Antioquia in Colombia, Massachusetts General Hospital, and the Shepens Eye Institute of Massachusetts Ophthalmology, to study the patient’s condition. generously allowed. 1,200 relatives have undergone extensive genetic testing, brain imaging, and postmortem brain tissue, according to the report. journal natural medicine.
of problem patient Presenilin 1 (dog 1), known to cause mild cognitive impairment (MCI) by a median age of 44 years and dementia by 49 years. However, until age 67, he was cognitively normal, and by age 70 he did not develop MCI or mild dementia by age 72.
The answer to why this man was able to ward off disease for so long lies, at least in part, in his genes. In addition to the Alzheimer’s disease-causing mutation, the man had a newly reported mutation in the RELN gene. Reelin-Corvoswhich appears to provide protection from Alzheimer’s disease. His sister, who also has the same genetic risk, was found to have a mutation in another protective gene. She avoided her cognitive decline until her age of 58 and dementia until her age of 61.
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It is well known that people with Alzheimer’s disease have an accumulation of a protein called Alzheimer’s disease. amyloid in their brain. A group of amyloid proteins called plaques are thought to be responsible for the disease, and many Alzheimer’s drugs target amyloid. However, the case revealed that both brother and sister had high levels of amyloid plaques in their brains, yet showed no signs of cognitive decline or dementia.
Examining how protective mutations work provides new insights into the pathogenesis of Alzheimer’s disease. Protective Reelin-COLBOS mutations connect to receptors in brain cells, Reduces activation of a protein called tau, are known to form tangles in the Alzheimer’s disease brain. Remarkably, imaging studies of this man’s brain showed few tau tangles in the brain region, despite the presence of numerous amyloid plaques. entorhinal cortex. If there is a mutation in another gene, Apoe, Connecting to its receptors instead increases tau activation and accelerates the progression of their tangles and cognitive decline.
This new genetic information Researchers may change their minds and develop a cure for this disease.
A female chemist working in a laboratory.
This approach has already been successful in other areas of medicine. for example, women with very low cholesterol It turned out that she had a genetic mutation from her parents that caused her LDL cholesterol level to rise to a staggering 14. Researchers studied this rare mutation and how it works, and used the information to: Develop drugs to treat patients with very high cholesterol levels.
The same may one day apply to Alzheimer’s disease.Discovering, understanding, replicating, and mimicking the action of protective mutations may be the key to generating more mutations. Precision medicine Prevents the development of Alzheimer’s disease and other diseases.
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Sources 2/ https://www.forbes.com/sites/ellenmatloff/2023/05/22/man-defies-early-onset-alzheimers-could-hold-clues-for-treatment/ The mention sources can contact us to remove/changing this article |
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