Alzheimer ’s disease was the seventh with child cause of destruction in the US last year . As life expectancies rise andanti - aging researchlooks to bear on human past their instinctive limits , it will only worsen an subsist problem – in fact , the figure of cases is await todouble every 20 yearsuntil it off an amazing 139 million the great unwashed live with dementia in 2050 . Yet despite scientists ’ better effort , every unmarried dementia drug neglect .
Most latterly , the long - look to drugcrenezumab , which targets amyloid brass , failed clinical trial , proving unable to demonstrate any significant advance in people with transmitted Alzheimer ’s . Disappointment was far-flung , yet those familiar with the field were unsurprised , jaded by years of similar results .
So , what is it about Alzheimer ’s that do it so punishing to puzzle out ?
A number of estimation have been put forward . It may be that our fauna models are inherently blemished : mouse that scientists mastermind to have an Alzheimer’s - corresponding phenotype might not actually have the disease ( after all , it ’s voiceless to narrate whether animals have mental capacity disorderliness at the in force of times ) .
instead , most research rivet on amyloid plaques , which are soma - ups of mis - close down proteins thought to block signal in the brain . However , it persist without any definitive validation whether these plaque cause Alzheimer ’s , or whether they exist simply as a consequence . All we have a go at it is that they are a clear characteristic within the brains of hoi polloi with the disease and that they can do nerve cell damage .
A shift in strategy
Now , a group of investigator are suggesting it may be time to pitch focus away from creating a miracle drug that staunch Alzheimer ’s in its track , and instead turn our attention to things we do fuck , such as behavioral risk factors that have been proven to increase peril . mellow blood atmospheric pressure , smoking , and learn expiration are all highly implicated in the development of Alzheimer ’s , so what if policy pitch to bar rather of cure ?
That is the argument of a new study of late published inJAMA Neurology , which has found that a orotund identification number of dementedness cases in the US could have been preclude if lifestyle peril factors were reduced , based on their determination .
Specifically , the study looked at 16,690 player from across the US , including some information from Asian and Pacific Islander backgrounds , to tax risk scores of various behavioral traits . They then generated population attributable fractions ( PAFs ) for each risk factor , representing the per centum of US dementedness case that would be forbid if this hazard was eliminated .
Hypertension came out as the unclouded leader , with a staggering 12.4 percent of dementedness cases being preventable if high blood pressure was solved . Hearing loss also represent a function with a more small 1.8 per centum , but when adjust for the huge phone number of dementia cases across the US , this represents around 100,000 preventable cases each twelvemonth if it was targeted with readily - available discourse .
According to one psychiatrist speaking toThe New York Times , it is fourth dimension we shifted policy towards keep risk gene . Their work suggest that up to 40 pct of all dementia cases could be a termination of 12 preventable or treatable lifestyle factors .
“ A monolithic alteration could be made in the number of people with dementia , ” tell Dr Gill Livingston , chairwoman of the Lancet Commission onDementia prevention , intervention , and care .
“ Even small percentages – because so many the great unwashed have dementia and it ’s so expensive – can make a vast departure to person and families , and to the economy . ”
