Should we be curing or caring?

“In these pictures we see with heart-breaking intensity William’s efforts to explain his altered self, his fears and his sadness. The great talent remains, but the method changes. He sometimes uses water-colour and paints a series of masks, perhaps because he could more quickly express his fear. In both the oils and water-colours these marvellous self portraits express his desperate attempt to understand his condition. There is a new freedom of expression, the paint is applied more thickly, art-historically speaking the artist seems less linear and classical, more expressionist, and I see ghosts of his German heritage.” — Patricia Utermohlen, widow of artist William Utermohlen

Theories of Alzheimer’s disease as a distinct disease entity from senile dementia or even pre-senile dementia have been argued for over a century. The results of clinical trials have identified several medical conditions heralded by the presence of plaques and tangles in the absence of cognitive dysfunction as identified as potentially causative in patients diagnosed with Alzheimer’s. David Rothschild MD, a US psychiatrist postulated in a 1936 article in the Archives of Neurology & Psychiatry that perhaps what we see as a separate disease entity is actually a generalized tissue reaction derived from multiple biologic pathways.

As research advances are reported, the lack of consensus on the role of amyloid plaques or a single casuative disease entity isn’t typically introduced into the conversation. Perhaps the willingness to substantiate a somatic vs psychiatric role unique from senility or senescence hurried a distinction that better fit the model of a pharmaceutical enterprise. How can the pathology of Alzheimer’s Disease be validated as distinct from neural aging and senescence in the absence of a single biologic marker?

Since renewed interest in Alzheimer’s Disease research in the 1970s neither a cure nor an effective method of prevention has been developed. Research findings indicate a multifactorial and complex etiology but why is the way forward so linked to the role of plaques in the brain? The diagnosis is only confirmed post-mortem by detection of amyloid beta plaques and neurofibrillary tangles (tau protein) however, non-demented, aged patients may have a histopathology that is indistinguishable from AD Additional microvascular changes, cellular hyperintensities as well as other findings that remain outside the accepted standards of pathognomonic metrics have also been detected.

Changes in the brain that ultimately produce the symptoms of Alzheimer disease begin many years, perhaps decades, before Alzheimer dementia can be diagnosed. If these changes can be reliably detected in living persons, it may identify those individuals who are at great risk of developing dementia in future years and who also may be an ideal group of individuals to participate in prevention studies of Alzheimer dementia.

I read interviews with the leading researchers of our day that contribute quite a bit to our understanding of the challenges ahead in managing the billion dollar healthcare costs of Alzheimer’s Disease but I can’t seem to disconnect from the multifactorial process in general and normal neuropathic aging of the brain.

The main driver of the increased research efforts, however, is the rapidly aging population. The older adult population has increased greatly since the 1970s, not just in the US, but worldwide, and continues to grow. The “baby boomers” have just started turning 65 and are at the forefront of a tremendous demographic revolution that will result in the graying of America. The public health consequences will be enormous. Medicare already is strained and will be overwhelmed by the number of people in the next 10 to 15 years who reach the ages at which Alzheimer’s disease is most prevalent. As they develop the illness, our capacity to care for them will be exceeded. There thus is a very strong imperative to devote all resources needed to conquer Alzheimer’s. — John C. Morris, M.D.

Should we actually be devoting all of our resources to curing Alzheimer’s Disease or should we be looking for links between social determinants of health, aging, and brain health. Perhaps we should be more focused on caring vs. curing?

If Alzheimer’s disease is a diffuse clinical syndrome, there is unlikely to be a therapeutic silver bullet, notwithstanding the dominant research endeavour towards finding effective drug treatments. But if “what is good for our hearts is also good for our heads,” should we be equally focusing on reducing cardiovascular risk? Yes of course; this is a public health goal in its own right. But an integrative public health strategy should also recognise that risk of Alzheimer’s disease evolves throughout life. This approach would target risk of insults to the brain beginning in the uterus, during childhood poverty and its consequences such as overcrowding and inadequate nutrition, through poor schooling, risky lifestyle; and through effects of low attainment such as hazardous occupational exposures and chronic stress. Although the life course process is also associated with cumulative risk of chronic physical diseases that are linked to Alzheimer’s disease, such an outlook goes beyond the medical dimension as an approach to labelling and intervention in Alzheimer’s disease. — What Do We Mean By Alzheimer’s Disease?

More to come…stay tuned

Originally published at

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