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Dec. 2, 2020 | Wednesday
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Dr. Brown: Slow progress on Alzheimer’s
File photo.

Dr. William Brown is a professor of neurology at McMaster University and co-founder of the Infohealth series at the Niagara-on-the-Lake Public Library.  


Dr. William Brown
Special to The Lake Report

My wife, now 77 and living in a NOTL nursing home, showed the earliest signs of dementia of the Alzheimer type more than 10 years before – signs of which family members, friends and I barely took notice at the outset.

Those signs became evident to all in later years, when working backward, we compared notes with one another and recalled the earliest memory lapses, mistakes in weaving which she would never have made before, which became increasingly common and frustrating. There also were subtle difficulties keeping track of financial accounts and calendar events.

An outgoing person by nature, only later in the disease did she begin to lose some of her natural confidence and enjoyment of people. 

These and other signs strongly suggest the cognitive and behavioural declines associated with Alzheimer’s disease begin much earlier than most patients, their families and family physicians are aware and much earlier than all but the most discriminating neuropsychological tests might reveal.

However, PET (positron emission tomography) scans and studies of the cerebrospinal fluid reveal a different picture; amyloid deposits in the brain and elevated amyloid in the cerebrospinal fluid one or two decades before the first obvious symptoms attributable to Alzheimer’s.

No surprise here – post-mortem studies of the brains of Alzheimer’s patients point to the loss of 30 to 50 per cent of the brain cells in selected regions, such as the hippocampus, and the attendant loss of all the related often widespread neural connections by this stage. 

Those PET and pathological observations make a compelling case for early intervention to protect the most vulnerable brain cells, long before the disease becomes clinically obvious, when it may be too late to intervene.

Unfortunately,  the Alzheimer world crashed a year ago because trial after trial of drugs designed to forestall or slow the buildup of amyloid and thus it was hoped, progression of the disease, failed. It was the end of a global 10-year investment in the amyloid hypothesis as the cause of Alzheimer’s and an example that in medicine we sometimes put all our eggs in one basket and when they crash, so do our hopes. 

Is tau, known to be responsible for the neurofibrillary tangles in Alzheimer’s, the primary cause of the disease or yet another investigative mistake in the offing? (* See note below.)  Are we missing a more basic cause that might have little to do with amyloid or tau? At this point we don’t know.

That’s unfortunate as clinical trials in AD are very expensive because of the need, until now, for PET scans and for some trials, cerebrospinal fluid analysis for amyloid and tau. That’s where the good news comes in. 


Recently, blood tests for tau have been developed which apparently are as sensitive as PET scans and cerebrospinal fluid studies for identifying Alzheimer’s. That’s a huge plus if the claims are supported, because reliable blood tests would make future clinical trials, especially for those in the very early stages of Alzheimer’s, much cheaper and easier for patients and families. 

There is hope on the horizon – hope many, including me – thought was dashed by the dismal outcome of so many promising drugs for Alzheimer’s.

* NOTE: At the end of my neurology training in Toronto, I was involved in research on Alzheimer’s. The project involved using aluminium to induce the pathological hallmarks of the disease in the brains and spinal cords of cats to learn whether cells jam-packed with neurofibrillary tangles, functioned normally, or not.  At the end of the study, which involved recording from single motor nerve cells in the spinal cord, every one of which had tangles, the findings weren’t at all what I expected. Every single one of those cells behaved normally despite the tangles. Hence, I’ve been skeptical of the amyloid and tau hypotheses since they emerged several decades ago. And if you’re wondering whether I would consider repeating a study like that on cats – of course not.

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