why don’t we have a cure for alzheimer’s?

over the past year, scientists have tackled covid-19, a previously unknown disease and within months developed effective new vaccines.  over that same time frame , the list of  alzheimer’s treatment failures got longer . currently,  the only approved drugs for alzheimer’s  merely alleviate some of the symptoms — partially and temporarily — but do not stop the disease from progressing.

although it was first officially  described 115 years ago , and of course existed long before that, we still do not have a cure for this devastating disease. why?

let’s start by following the money. for years, patient advocates have pointed to the escalating toll and ballooning costs of alzheimer’s as the world’s population ages.  alzheimer’s is severely underfunded  in comparison to cancer, heart disease, hiv/aids and even covid-19.

sadly, the mistaken belief that alzheimer’s only affects older people is a contributing factor to this underfunding. however,  five to 10 per cent of people with alzheimer’s are under 65 years of age ; some are even in their 40s. alzheimer’s is also a disease of the entire family, causing  anxiety, depression and exhaustion in caregivers  and loved ones, exacting a disproportionately high socio-economic cost.

the most time-honoured theory is that alzheimer’s is caused by  misfolded proteins  that aggregate or clump, killing brain cells and giving rise to the symptoms of memory loss and reduced cognition. initially, the culprit in this misfolding story was a protein called beta-amyloid. more recently, another protein, tau, has emerged as a possible contributor.

although a wealth of research data have supported this protein misfolding theory, referred to as the amyloid hypothesis,  multiple drugs designed to block the brain’s toxic protein misfolding processes have failed in human trials, repeatedly . in fact,  in the past two years , several major clinical trials  based on the field’s leading hypothesis  — that reducing the level of aggregated beta-amyloid that riddles the brains of alzheimer’s patients would halt disease progression — have dramatically failed.

and so there are many other theories.  a new heavyweight contender is the neuroinflammation theory  of alzheimer’s which suggests that the disease arises from an excessive release of toxic  inflammatory chemicals from immune cells in the brain  called microglia. drugs designed to address this theory are fundamentally different from those addressing the amyloid hypothesis, and are still early in the developmental process.

a different theory claims that alzheimer’s is a  disease of synapses , which are the junctions between brain cells, and yet another suggests that alzheimer’s is a  disease of mitochondria , a structure central to energy production in every brain cell.

the path towards a cure is not going to be easy, and even if these theories do lead to the development of drugs,  these drugs may fail for a host of other reasons .

one final problem is that alzheimer’s may not simply be one disease.  it may in fact be a collection of similar diseases . a 52-year-old with early onset alzheimer’s certainly has a clinical course distinct and different from an 82-year-old with late onset alzheimer’s. will a drug that works in an 82-year-old also work in a 52-year-old person’s disease? maybe, or maybe not.