Alzheimer’s disease has followed Doug Whitney around like a ‘plague.’
Mr Whitney, from Washington state, grew up with more than a dozen aunts and uncles, but 10 didn’t make it to their 60th birthdays.
They all inherited a faulty gene that is virtually guaranteed to cause Alzheimer’s disease, the most common form of memory-robbing dementia.
But at 75, Mr Whitney still shows no signs of the condition.
Experts believe he is one of just three ‘exceptional resilience mutation carriers’ in the world to escape this genetic destiny.
Now a team of scientists in Missouri is working to figure out how his brain protected him against the disease that afflicts nearly 7million Americans.
While the cause is still unclear, researchers in a new study suggest it could be due to high levels of protective proteins in his brain from working in hot conditions during his 20-year Navy service.
These ‘hot shock proteins’ may prevent the toxic proteins from building up and killing brain cells.
Doug Whitney (pictured above with his wife), a 75-year-old Navy veteran from Washington State, has evaded Alzheimer’s disease, despite inheriting a gene that almost guarantees the condition. Experts at Washington University in St Louis are working to figure out how
Projected yearly incidence of dementia on the basis of current rates (solid lines) and projected incidence of dementia assuming continuation of a decreasing trend (dashed lines)
Dr Jorge Llibre-Guerra, an assistant professor of neurology at Washington University in St Louis, said: ‘If we are able to uncover the mechanism behind this resilience, we could try to replicate it with a targeted therapy designed to delay or prevent the onset of Alzheimer’s, leveraging the same protective factors that have kept Mr Whitney from developing this disease to benefit others.’
Alzheimer’s disease is the most common form of dementia, a group of neurological disorders that impact memory, language, problem-solving, and other cognitive abilities.
About one in nine Americans over age 65 will be diagnosed wth Alzheimer’s, and two-thirds of patients are women.
The disease is caused by toxic proteins beta amyloid and tau, which accumulate in the brain and form plaques that disrupt neurons and kill brain cells.
Mr Whitney’s family members make up the less than one percent of Alzheimer’s patients who inherited a specific gene that almost always results in Alzheimer’s.
All of these family members carried a mutated version of the gene presenilin 2 (PSEN2), which causes them to develop excess levels of beta amyloid and tau proteins.
When Mr Whitney turned 60 and still hadn’t developed Alzheimer’s symptoms, he assumed the gene hadn’t been passed on to him.
However, he volunteered for Washington University’s Dominantly Inherited Alzheimer Network (DIAN) study in 2011 in an effort to help others. Researchers found he had indeed inherited the faulty PSEN2 gene.
Dr Llibre-Guerra said: ‘It came as a big surprise to learn that he was actually a mutation carrier.
‘At that point, he earned the title of the DIAN escapee because he was actually able to escape the expected course of the disease.’
Mr Whitney grew up with more than a dozen aunts and uncles, but 10 didn’t make it to their 60th birthdays
The above map shows rates of Alzheimer’s disease by US county in people over 65 in 2020
Mr Whitney was the subject of a new study in the journal Nature Medicine.
Scans of his brain showed a significant amount of amyloid proteins, but there was only a small concentration of phosphorylated tau in his left occipital lobe, which sits at the back of the skull.
The researchers said that in inherited Alzheimer’s cases, phosphorylated tau usually spreads to multiple areas of the brain, and symptoms are most pronounced in the medial temporal lobe, which controls stores long-term memories.
Dr Randall J Bateman, co-senior study author and DIAN director at WashU Medicine, said: ‘The goal now is to discover the precise reason why Mr Whitney has escaped genetic fate.
‘This discovery could become a powerful prevention for everyone. We call on researchers to help in the search.’
Further tests revealed Mr Whitney had high levels of heat shock proteins, which form in stressful conditions like heat, cold, radiation, and infection.
It’s thought that these proteins act as ‘chaperones’ for proteins, helping them form and fold correctly. This prevents folded proteins associated with brain cell damage.
The experts believe Mr Whitney may have cheated his fate during the 20 years he spent as a shipboard mechanic in the Navy.
This work involved long periods of time withstanding temperatures as high as 110 degrees, which could have caused the elevated heat shock proteins.
Later this year, Mr Whitney will travel from Washington to St Louis again for additional testing in hopes of learning how to protect others from Alzheimer’s disease.
He said: ‘My family has been devastated by this disease since the early 1900s, and probably going back further than that.
‘It’s really important to me to figure this out.’
