A man managed to ward off Alzheimer’s thanks to his natural immunity, despite having a gene that made him more susceptible – making him the second known case.
A team of international scientists found that the Colombian man, who was predicted to have dementia in his 40s, was also a carrier a rare genetic variation that helped protect him from the debilitating memory disorder.
The man died at the age of 74 with only moderate dementia.
Researchers hope their findings can lead them to specific areas of the brain where the disease can be stopped or delayed, giving hope to 6.7 million Americans with Alzheimer’s disease.
It’s because scientists at the Massachusetts Institute of Technology (MIT) discovered a new way to reverse Alzheimer’s disease by using ashchain of amino acids to interfere with an enzyme in mice that is typically overactive in the brains of people with the disease.
The Colombian man was found to have a mutation in a gene called reelin, which could explain why he can stay dementia-free for another 20 years
The man, a former mechanic from Colombia, inherited the Paia gene mutation when he was born, predicting the disease would have killed him in his 60s.
This mutation is the most common cause of early onset Alzheimer’s disease and is commonly found in people living in Colombia.
Mild cognitive impairment begins around age 45 and dementia around age 50.
Instead, the man was studied by the scientists continued resilience and retired in his early 60s before passing away in 2019 at age 74.
The man was first examined by neurologists at age 67, who found he was cognitively normal, and neither he nor his family were concerned about his memory.
He is only the second patient ever to resist the powers of the Alzheimer’s gene, a team of scientists write in the journal Naturopathy said.
Researchers scoured his genome to find another mutation that may have protected him from the disease.
The team found that the man had a mutation in a gene that codes for a protein called reelin, which is associated with brain disorders, including schizophrenia and autism.
However, the protein may have saved the man from dementia, as his brain looked like someone riddled with the disease.
The team found that the man had a mutation in a gene that codes for a protein called reelin, which is associated with brain disorders, including schizophrenia and autism.
He had the hallmark signs of Alzheimer’s disease, including amyloid plaques and tau tangles in his brain, but he had a limited number of tau tangles in his entorhinal cortex, which is essential for memory.
Joseph Arboleda-Velasquez, an associate scientist at Mass Eye and Ear, a Harvard teaching hospital, and one of the study’s leaders, told the Washington Post: ‘I think it’s important that we listen to the patients. And I think what the patients are telling us is… there is a path to protection.”
He said: ‘The genetic variant we identified points to a pathway that can produce extreme resilience and protection against the symptoms of Alzheimer’s disease.
‘Without patients we wouldn’t be able to get these kinds of insights. They show us what’s important when it comes to protection and challenge many of the field’s assumptions about Alzheimer’s disease and its progression.”
He added, “The possibility that you can get that protection just by protecting the entorhinal cortex, even if you have a lot of Alzheimer’s elsewhere? Wouldn’t that be great? That’s so tempting.’
In 2019, researchers discovered a woman, Aliria Rosa Piedrahita de Villegas, who avoided dementia until she was 70.
She was found to have another genetic mutation that kept Alzheimer’s at bay, known as Christchurch.
While her brain showed a lot of amyloid plaques typically found in Alzheimer’s patients, it didn’t have the tau tangles also associated with the condition.
Doctors hope the cases will open up new treatments for the disease, but recognize there could be multiple factors contributing to extending the life of a person’s memory rather than a single explanation.