IT is well over 100 years since Alois Alzheimer first described what he called an “unusual disease of the cerebral cortex”.
The German pathologist and psychiatrist presented his findings at the 37th Congress of Psychiatrists in 1906 after carrying out a post-mortem on the brain of one of his patients, Auguste Deter, who had been plagued by worsening confusion, memory loss, and hallucinations over a period of five years until her death aged 50.
Her brain, he discovered, was riddled by distinctive protein clumps and nerve tangles never previously identified.
READ MORE: Seven things you might not know about dementia
Today, it is thought that these clumps - beta-amyloid plaques - accumulate to a certain “tipping point” which then triggers a rapid spread of another protein, tau, which block neurons from working properly.
It elicited little scientific interest at the time, however, and Alzheimer would die from complications of cold in 1915 long before the disease which bears his name became - thanks to an ageing population - one of the biggest healthcare challenges of our time.
By 2031, it is projected that there will be 102,000 to 114,000 people living with dementia in Scotland - an increase of 75 per cent compared to 2007 levels. Alzheimer’s, the most common form, affects around 60% of sufferers.
Until now, the only drugs available for the disease have helped to alleviate symptoms rather than tackling the underlying cause - but that could be about to change.
On Wednesday, scientists from around the world will converge in San Francisco for the CTAD Alzheimer Congress - an annual conference which brings together the latest results from clinical trials. The mood has never been more electric.
“I think this is a historic moment,” said Professor John Hardy, chair of molecular biology of neurological disease at University College London who is spending $7000 (£5,800) of his own lab’s money just to attend.
The cause of the excitement? A new antibody drug, lecanemab, which has been shown for the first time to remove amyloid build ups in the brains of Alzheimer’s patients.
This is said to equate to a 27% reduction in decline when given to patients with only mild cognitive impairment, and might be expected to translate into an extra 19 months of independent life on average.
READ MORE: The mystery of falling sperm counts that 'threatens mankind'
It is a modest gain, but for researchers it marks the first real turning point in the history of the disease.
“Amyloid therapies were first suggested in 1992 so that tells you how long it’s taken to get here,” said Prof Hardy.
“A lot of the earlier amyloid antibodies did not take amyloid out of the brain - they just prevented further build up - and those did not work.
“One swallow doesn’t make a Spring, but I’m excited about this. I think it might be the end of the beginning; I’m optimistic that we are seeing the beginning of Alzheimer’s therapies.”
Prof Hardy suggested that the breakthrough might eventually lead to a “brave new world” where people are routinely given cholesterol-style blood tests on their 60th birthdays to check their amyloid levels.
Those people whose amyloid is “on the way up” could be given drugs such as lecanemab to slow or prevent the onset of Alzheimer’s, said Prof Hardy.
For now, scientists are just eager to see the full clinical trial data unveiled in San Francisco. So far all we have are press releases from lecanemab’s manufacturer, Tokyo-based pharmaceutical firm Eisai.
It has also yet to be licensed for use. America’s FDA is set to rule on lecanemab in January 2023, with UK and European regulators to follow.
READ MORE: NHS executives warn that current model is 'no longer working'
Already, however, charities and clinicians are warning that a major shake up of how the NHS diagnoses Alzheimer’s will be imperative to maximise any benefit from the drug, which has to be administered at an early stage.
“Most of the patients who get referred to us at the moment have later symptoms because our health system is set up to keep people with early symptoms out of secondary care and out of the memory clinics,” said Dr Liz Coulthard, an associate professor of dementia neurology based in Bristol.
In addition, fewer than 1% of patients seen by UK dementia clinics have a precise diagnosis of Alzheimer’s disease, which is crucial to determining eligibility for lecanemab.
Other forms of dementia, such as vascular or Lewy-Body, are not caused by amyloid build ups.
Currently the only way to achieve a definitive diagnosis of Alzheimer’s is by lumbar puncture to extract spinal fluid which can then be analysed for the amyloid biomarker, or through brain PET scans.
Blood biomarker tests for amyloid are “just on the horizon”, said Dr Coutlhard, and would be “really helpful”.
In the short-term, however, she envisions lecanemab operating as a “parallel service” to existing dementia care.
She said: “I don’t think in the short term there is going to be a reduction in the need for post-diagnostic care so we need new personnel and funding.
"Where that’s going to come from in the current climate, I don’t know.
“It very much depends if there a licence [for lecanemab], who the licence is for, and what the MRI guidance is.
"We’re very likely to have to do one or two MRIs, which is more than most patients currently get, and we’re going to need to do biomarker testing which is currently only done in the major centres.”
MRIs are needed to monitor patients for bleeding and swelling on the brain, which can be a side effect of lecanemab but tends to be symptomatic only in around 3% of patients.
More detail is also needed on who is most at risk of these brain changes, said Dr Coulthard - adding that this will be “really important to look out for at CTAD”.
Whatever the obstacles, we are on the brink of a “momentous occasion”, said Dr Susan Kohlhaas - director of research for Alzheimer’s Research UK - because lecanemab “disproves the myth that Alzheimer’s is an inevitable part of ageing”.
She added: “Getting people diagnosed early and into research early will be really important in the coming years. This is a real window of opportunity.”
Why are you making commenting on The Herald only available to subscribers?
It should have been a safe space for informed debate, somewhere for readers to discuss issues around the biggest stories of the day, but all too often the below the line comments on most websites have become bogged down by off-topic discussions and abuse.
heraldscotland.com is tackling this problem by allowing only subscribers to comment.
We are doing this to improve the experience for our loyal readers and we believe it will reduce the ability of trolls and troublemakers, who occasionally find their way onto our site, to abuse our journalists and readers. We also hope it will help the comments section fulfil its promise as a part of Scotland's conversation with itself.
We are lucky at The Herald. We are read by an informed, educated readership who can add their knowledge and insights to our stories.
That is invaluable.
We are making the subscriber-only change to support our valued readers, who tell us they don't want the site cluttered up with irrelevant comments, untruths and abuse.
In the past, the journalist’s job was to collect and distribute information to the audience. Technology means that readers can shape a discussion. We look forward to hearing from you on heraldscotland.com
Comments & Moderation
Readers’ comments: You are personally liable for the content of any comments you upload to this website, so please act responsibly. We do not pre-moderate or monitor readers’ comments appearing on our websites, but we do post-moderate in response to complaints we receive or otherwise when a potential problem comes to our attention. You can make a complaint by using the ‘report this post’ link . We may then apply our discretion under the user terms to amend or delete comments.
Post moderation is undertaken full-time 9am-6pm on weekdays, and on a part-time basis outwith those hours.
Read the rules here