Alzheimer’s ‘vaccine’ set for human trials

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An Alzheimer’s ‘vaccine’ is about to be tested in a series of human trials in Australia and the US.

Flinders University Professor Nikolai Petrovsky said researchers had completed successful testing on mice, which had been “genetically programmed to get dementia and Alzheimer’s disease”. He explained that the team had been able to prevent memory loss in the mice and that the next step was to take this into human clinical trials – hopefully in the next 18 to 24 months.

“It’s an exciting time to be starting the new decade. Hopefully this is the breakthrough of the next decade if we can get it to work in the human trials,” he told ABC Radio Adelaide.

“It’s an exciting juncture.”

The vaccine was developed by Prof. Petrovsky in research being led and funded by the Institute for Molecular Medicine and University of California, in the US.

“Currently, we believe Alzheimer’s disease is caused by a build-up of abnormal clumps of protein in the brain,” he said.

“It’s like they gum up the system, a bit like when your pipes get blocked and they don’t work so well.

“The same thing happens in the brain with Alzheimer’s. You get these build-ups of clumps of protein between the brain cells and they start to interfere with the communication between the brain cells.

“With the vaccine, what we’re doing is getting the immune system to make antibodies that can recognise those abnormal clumps of protein and will actually pull them out of the system and break them down.

“It will unblock the pipes and let the brain go back to normal.”

However, a new study from the University of California and the Veterans Affairs San Diego Healthcare System argues that the build-up of the beta-amyloid protein may not cause Alzheimer’s.

The research involved 747 participants with different levels of cognitive health who agreed to undergo neuropsychological assessments, as well as PET and MRI brain scans. Of that group, 305 were cognitively healthy, 289 had mild cognitive impairment and 153 displayed markers of what the investigators called “objectively defined subtle cognitive difficulties (Obj-SCD).

The investigators defined participants with Obj-SCD as those who showed “difficulties or inefficiencies on some sensitive cognitive tasks” even though their overall neuropsychological profile was considered to be in the normal range.

In a paper in the journal Neurology, senior author Professor Mark Bondi said brain scans of people with Obj-SCD showed that they experienced a thinning of brain matter in the entorhinal cortex – the area that plays a role in memory and spatial orientation – before significant levels of amyloid had accumulated.”

First author Dr Kelsey Thomas said the new findings could help to refocus research.

“A method of identifying individuals at risk of progression to [Alzheimer’s disease] using neuropsychological measures has the potential to improve early detection in those who may otherwise not be eligible for more expensive or invasive screening,” he said.

Dementia is the second leading cause of death of Australians and in 2016 became the leading cause of death of Australian women.

In 2019, there were an estimated 447,115 Australians living with dementia, according to, and without a medical breakthrough that number is expected to increase to 589,807 by 2028 and 1,076,129 by 2058.

Do you closely follow developments in this area? Are you concerned about what might be in store?

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Written by Janelle Ward


Total Comments: 11
  1. 0

    No thanks.

  2. 0

    My mum died from Alzheimer’s and my father from MSA (Multiple System Atrophy) both neurological diseases. So yes I am particularly interested.

  3. 0

    Yes. Yes., very concerned. I received a card this Christmas from Alzheimer’s Australia, it said, “Happy Easter”….

  4. 0

    I’d be dubious about trying a vaccine for Alzheimers… I’ve read widely about Alzheimers because I’m a live-in carer for someone with Alzheimers. It’s true the plaque and tangles theory dominates the research, but if you delve deeper into the journals, the evidence doesn’t conclusively support this theory. For instance autopsies have been done on deceased elderly people and their brains still had plaques and tangles but these elderly people did not show any clinical indications of having Alzheimers when they were alive. So the observation of plaques and tangles in a lot of people with Alzheimers might be just a symptom that the brain is battling inflammation – rather than the “cause” of Alzheimer’s – (meaning a vaccine is pointless.)

    There’s also an observed genetic predisposition to Alzheimer’s that runs in some families – (again a vaccine can’t alter someone’s genes.) Except having the gene doesn’t mean you will definitely develop Alzheimer’s. And people without the gene also get Alzheimers.

    The diet/lifestyle argument is another theory. Now that more and more seniors are developing Alzheimer’s, some researchers are concentrating their efforts on comparing the lifestyles of seniors who’ve developed Alzheimers compared to seniors of the same age who haven’t developed it. It’s too early to reach any conclusions, but the crude patterns are curious. Apparently the highest rate of Alzheimers is in Finland – and Finland has also been aggressively promoting the low fat, low cholesterol, take your cholesterol medication, no sugar, take your sugar alternatives, no salt, take your salt replacement diet/lifestyle for the last 25 years. Do your own research but the gist of the trends are – Seniors with Alzheimers have a history of frequent doctor visits, and taking multiple daily medications that may unintentionally interact e.g. cholesterol lowering statins, hormone replace therapy, arthritis medication,painkillers like codeine, ibroprofen and panadol. Whereas those without Alzheimer’s reluctantly go to the doctor, they only use essential medication on a daily basis and they rarely use painkillers. Another difference is those with Alzheimer’s have a history of using products with aluminium e.g. hair dyes, perms, perfumes; they also are more likely to have annual flu shots than those without Alzheiemer’s ( Youtube the chemical reaction between mercury and aluminium if you don’t understand the significance of this difference). There are also emerging subtle diet differences – those who have developed Alzheimers are more likely to have spent years on a low fat, low cholesterol diet and they’ve commonly used low fat milk, artificial sweeteners, diet coke, diet pills, salt alternatives and soy and margarine. They’ve also eaten take-away meals 1-2 times a week. Whereas seniors with healthy brains tended to eat simpler homemade food – stews, home grown veggies, they’ve used regular salt, butter, sugar, whole fat milk, and prefer water or home made cordial than soft drinks. They also rarely buy takeaway or eat out. So there might be a chemical “cause” behind Alzheimers. And the fact that it’s observed to run in some families might be because family members copy other member’s lifestyles and diets.

    • 0

      What a great comment!
      I agree with you and it has been observed that people who have a high dietary intake of sugars like sweets, cakes, biscuits and lemonade and Coles end up with dementia!
      THIS IS also noted by nurses when we see so many elderly dementia patients and aged care facilities residents with dementia absolutely LOVE DESSERTS!
      They will not eat their main courses in many cases or will eat their desserts before they have a little bit of their mains so anyone reading this and is falling into or is in this category, would be well advised to eat more fruit and vegetables, proteins and whole grain cereals!

    • 0

      EXCESSIVE ALCOHOL IS ANOTHER LEADING CAUSE OF DEMENTIA in many but genetics may be a causal factor, however, if not dementia then heart attacks or strokes will strike one, even if not overweight!

  5. 0

    Any news is good news about this disorder.
    I found Aussie Carers’ comments both interesting and informative, it’s gone into my files!



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