Early enthusiasm for the new dementia drugs, lecanemab and donamab, hasn’t been matched by enthusiasm by governments around the world to pick up the tab. I find out why.
Main Points
- ‘Symptom-modifying’ drugs have been around for more than 20 years;
- ‘Disease-modifying’ drugs are new; those that reduce amyloid were hailed as ‘momentous’;
- Most governments approved the old & new drugs but, apart from the USA, will only pay for the old;
- Based on the evidence, perhaps this is good news – as is the choice of alternatives.
The Old Ones
Before we go to the ‘new dementia drugs’, governments in Australia, NZ, the UK, Canada and the USA do pay for some dementia drugs – the older, inexpensive, short-term drugs that modify symptoms like confusion, memory loss and agitation.
These older drugs include donepezil (commercial name Aricept), rivastigmine (Exelon) and galantamine (Razadyne) whose approvals date back to 1996. They’re regarded as ‘short-term’ because they provide some relief for symptoms of early-stage dementia, but become less effective as the disease progresses.
That’s why, in the early 2000s, researchers sought drugs that would impact the disease – not just the symptoms – and be safe.
The first ‘disease-modifying’ dementia drug, Tacrine, had been approved before this is in 1993, but was withdrawn because it was neither effective nor safe. It’s not one of the ‘new dementia drugs’.
Aricept (donepezil) can help improve attention, memory, behavior, and the ability to do daily activities in dementia patients.
Aricept is not a cure for Alzheimer’s disease; it may help improve symptoms, but the condition will progress over time, even in people who take this medicine.
‘Momentous’ Breakthrough
In 2022, it was 29 years since Tacrine’s approval and one year since the second disease-modifying drug, aducanemab had been withdrawn from market. It was written off by its maker, Biogen-Eisai, because of persistent reports of low efficacy and too-high adverse effects.
So, when lecanemab (commercial name ‘leqembi’) appeared in 2022 and showed a slowing of cognitive decline by 27% over 18 months, neurologists and researchers were understandably excited. (It was – and still is – made by the same company as aducanemab and works the same way.)
- Alzheimer’s Research UK called it ‘momentous’
- Prof Sir John Hardy (UCL Queen Square Institute of Neurology) said: ‘It’s exciting to think that future work will build on this, and we will soon have life-changing treatments to tackle this disease.’
- Prof Tara Spires-Jones (University of Edinburgh) said the results were ‘a big deal because we’ve had a 100% failure rate for a long time’. Indeed, three decades.
Experts equated the slowing in cognitive decline to an extra 19 months of independent living.
When donanemab (commercial name Kisunla made by Eli Lilly) upped the ante in 2023 to 35% slower cognitive decline over 18 months, the excitement mounted.
- Prof Sean Kennelly (Tallaght University Hospital, said: ‘I think we could get to a stage whereby we can manage dementia like we do HIV…’
- Prof Sir John Hardy (UCL Queen Square Institute of Neurology) ‘Lecanemab and donanemab have shown us that slowing Alzheimer’s is possible, representing genuine progress… Today marks a truly exciting day for dementia research…’
- The Lancet: ‘We are in a new biological era of diagnosis and treatment for Alzheimer’s disease…’
By the way, although they use different monoclonal antibodies, (the mAb in aducanemab, lecanemab and donanemab) all three drugs do the same thing: they break down plaques of beta-amyloid, a protein in the brain, which are said to cause dementia.
That’s why these three drugs (and others in the pipeline using the same mode of action) are called ‘anti-amyloid drugs’. Lecanemab and denanemab are the two currently-approved drugs in this group. These are what I’m referring to as the ‘new dementia drugs’.
Despite their impressive performance figures – roughly 30% slower cognitive decline – by 2026, governments in Australia, the UK, Canada and New Zealand have not offered to pay for these momentous drugs. (In NZ, lecanemab has not yet been approved for use as of May 2026). Why?
‘Lecanemab and donanemab have shown us that slowing Alzheimer’s is possible, representing genuine progress… Today marks a truly exciting day for dementia research…’
Prof Sir John Hardy, UCL Queen Square Institute of Neurology
Why Are Governments Holding Back?
The Australian Therapeutic Goods Administration (TGA) approved donanemab (May 2025) before it approved lecanemab (September 2025) even though the former came out a year later; presumably it was donanemab’s superior 35% versus 27% slowdown figure.
Although both drugs can be sold and used here, this is the reason PBAC (Australia’s Pharmaceutical Benefits Advisory Body) said it wouldn’t add donanemab to the PBS:
‘While clinical trials demonstrated that donanemab can potentially delay the progression of early Alzheimer’s disease by approximately six weeks, the PBAC noted there is a lack of consensus among clinicians that these results would translate into meaningful improvements for patients…’
In other words, the benefits to patients weren’t high enough for the government to pay.
Did you notice that the 19 months had shrunk to just 6 weeks?
That’s because, looking more closely, independent reviewers found that the claims of 27% and 35% slowing of cognitive decline were relative to placebo, not per 100 patients. The absolute reduction was less than 3% over 18 months for both drugs, so living independently for even six weeks more as a result of taking these drugs, may be optimistic.
‘While clinical trials demonstrated that donanemab can potentially delay the progression of early Alzheimer’s disease by approximately six weeks, the PBAC noted there is a lack of consensus among clinicians that these results would translate into meaningful improvements for patients…’
Pharmaceutical Benefits Advisory Body (Australia)
(Questions about the science of anti-amyloid drugs here.)
Does Cost Come Into It?
It’s not just about performance. It’s a balancing act for governments of cost, benefit and safety.
In the USA where the government does shoulder the bill, the cost of lecanemab can be up to USD100,000 per person per year (donanemab is slightly higher) and most of it is not the cost of the drug. Here is how that figure was reached:
‘In addition to the company’s $26,500 annual price tag for the drug (lecanemab), treatment could cost U.S. taxpayers $82,500 per patient per year, on average, for genetic tests and frequent brain scans, safety monitoring, and other care’. (These are USD$)
Those scans and tests aren’t optional.
To be eligible to take the drug (government-subsidized or not) initial brain scans and genetic tests are required, followed by regular MRI scans to monitor adverse effects that include brain swelling and brain bleeding.
In others words, the tests and monitoring cost three times more than the drug and you can’t say ‘no thanks, I’ll have it without’.
Considering that dementia rates are going up around the world, you can see why many governments aren’t too keen to foot the bill – especially they may have to cover the drugs, plus all the extras.
‘In addition to the company’s $26,500 annual price tag for the drug (lecanemab), treatment could cost U.S. taxpayers $82,500 per patient per year, on average, for genetic tests and frequent brain scans, safety monitoring, and other care.
What Other Governments Did
The British National Institute for Health and Care Excellence (NICE) also didn’t add lecanemab and donanemab to the NHS.
In the UK, the cost per patients would be up to UKL90,000 for an 18-month course including administration. The NHS has now rejected these drugs three times, but the industry recommenced negotiations in early 2026, presumably, hoping to change this one day.
Canada’s drug agency adopted a similar stance to Oz and the UK for identical reasons. It approved both drugs but provided no financial support to patients.
The New Zealand government approved donanemab (the higher performer) but not lecanemab and won’t subsidise either, for the same reasons as the other jurisdictions.
In the USA, where the FDA was the first regulator to approve both drugs, private health insurance companies and government do cover some costs. Eligible patients may pay as little as 20% but eligibility criteria are complicated and insurance coverage varies widely. Authors in the linked analysis show how hard it is to work out final costs, especially when specialists, scans and tests are included.
The authors suggest that people who are eligible for government subsidy and have private insurance will likely be covered to some extent, but are unlikely to be the people most needing these drugs.
In other words, while these drugs are approved for use, it’s mostly those with deep pockets who can afford those extra six weeks of independent living.
It’s interesting to note that, after 18 months of use, most patients are still taking the drugs.
The results of Phase IV trials of these drugs – real-world feedback from typical people taking the drugs – may tell us more, if or when they’re published. If not, patients could be digging deep into their pockets for years, wondering when those six bonus weeks will start.
NICE opens consultation on previously-rejected Alzheimer’s treatments donanemab and lecanemab. The consultation follows an appeal by the manufacturers of donanemab and lecanemab after NICE said it would not recommend the drugs for NHS use for a third time.
Hesitation Backed By Science
Derk Lowe runs a commentary on drug discovery and the pharma industry at Science.org’s ‘In The Pipeline‘.
He’s been a researcher in the drug industry since 1989, working on projects from schizophrenia and Alzheimer’s disease to diabetes, osteoporosis and cancer.
Lowe doesn’t mince words, and Science,org makes it clear that his words are his own. The first questions Lowe asks are: Does it work and does it cause harm?
In relation to lecanemab and donanemab, he points out that ‘the improvements measured are actually far less than those seen with donepezil, a cholinesterase inhibitor that has been on the market for many years and which is considered a pretty weak stopgap therapy overall. donepezil slows the progression of the disease a little, in some people, for a little while – and these new antibodies, by all available evidence, are even less impressive than that.’
Donepezil is one of the symptom-modifying drugs I mentioned at the start.
Here are the current prices in Australia: Donepezil AUD180 a year (half this for pensioners) compared to AUD40,000 for lecanemab or AUD56,000 for donanemab (excluding tests, scans and specialists).
In other words, a ‘symptom modifying’ drug like donepezil is more effective than a ‘disease modifying’ drug that costs 200-times more. By the time the scans, tests and specialists are added, the ‘new dementia drugs’ could cost 500-times more than the old one that did a better job. (More about the questionable science of anti-amyloid drugs here.)
‘the improvements measured (from lecanemab and donanemab) are actually far less than those seen with donepezil …considered a pretty weak stopgap therapy overall.
What About Adverse Effects?
Lowe adds that ‘the safety situation is nowhere near as fuzzy as the efficacy numbers’ and quotes from an exhaustive review of lecanemab and donanemab by Alberto Espay and colleagues (that’s him at right).
‘With a disease as devastating as AD (Alzheimer’s Disease), even a small effect size should be considered by clinicians if treatments were safe. However, these monoclonal antibodies are not safe. In both trials, adverse events afflicted sizable numbers of participants. With lecanemab, 45% of patients had treatment-related adverse events, with nearly 1 in 4 developing brain swelling and/or bleeding … Severe bleeding occurred to a greater extent compared with placebo – 5 vs 1 in the lecanemab trial; 7 vs 2 in the donanemab trial – including three fatal cases.’
In short, nearly half lecanemab patients suffered adverse effects, but the number doubled for donanemab.
‘With donanemab, 89% of patients had treatment-related adverse events and more than one in three patients developed brain swelling and/or bleeding. Brain swelling is a major contributor to the acceleration of brain atrophy, a feature of most mAb (Alves et al., 2023).’
Lowe concludes that ‘This is not where we should be. The FDA should be approving therapies that make a difference in patient’s lives and which have a greater chance of helping them than hurting them. You’d think that would be the baseline. Instead, in Alzheimer’s, Duchenne muscular dystropy, and other areas we’re seeing a tendency to approve things on a “Wouldn’t it be nice” basis, which – to be a pain in the ass about it – is a route to disaster. The first criterion is always efficacy. Then you weigh safety against that.’
It’s a bit hard to disagree with Lowe’s reasoning or Espay’s figures which were taken from the original clinical studies.
With lecanemab, 45% of patients had treatment-related adverse events, with nearly 1 in 4 developing brain swelling and/or bleeding … With donanemab, 89% of patients had treatment-related adverse events and more than 1 in 3 patients developed brain swelling and/or bleeding…
What About Us Boomers?
In Oz, the UK, NZ and Canada, maybe we should be pleased that our governments aren’t wasting the tax dollars we gave them on expensive drugs that don’t work – and might even damage our precious brains. But where does it leave us, boomers?
We’ve been waiting patiently for answers for decades, but the dazzling light of amyloid-reducing drugs has vacuumed up research funds, diverted media attention and distracted governments. There’s been little opportunity to hear the quiet unsponsored voices of independent researchers who think chasing amyloid has been a complete waste of time.
The sad part is this: the moths burnt by amyloid’s bright flame aren’t the scientists who failed. It’s those of us who saw our loved ones left like empty shells discarded by cicadas.
Surely, There’s A Better Way?
Although the non-believers in amyloid are quiet of voice, their numbers are growing, as more evidence comes to light about non-drug-based ways to avoid the scourge of dementia.
These days, independent neuroscientists (who study how the brain works), neurologists (who study how to treat the brain) and other researchers believe that dementia can be prevented, delayed or even reversed – without the cost or adverse effects of amyloid-reducing drugs – or any drugs at all.
These and many functional medicine practitioners – who assess and treat whole patients, not just the symptoms they present – are convinced that dementia is something we can do something about.
They say that dementia (or Alzheimer’s which accounts for <70%) is not an inevitable part of ageing & we don’t have to get it.
These independent experts concur on these broad premises:
- Dementia is a metabolic disease; genes affect only 10% of cases;
- It’s caused by multiple factors, not accumulation of one protein in the brain;
- It develops over years, but improvements can be measured within months;
- Most of the causative factors are under our own control;
- In most cases, dementia can be prevented or delayed;
- If found early enough, dementia can be reversed.
If you’d more meat on these bones – to read how much these experts say you can do about dementia – you may like to see what’s inside Dementia: Keep Your Marbles, an eBook I wrote to try to make sense of all of this. It’s written in plain English with links to each research source. I update it continuously, too, so the current version always includes the latest research.
If you decide not to read further, that’s fine. It’s up to you. No pressure.
The good news is, according to independent sources, there a huge amount we can do about dementia, if we choose. We don’t have to sit, wait and hope. We can take action.
DEMENTIA:
KEEP YOUR MARBLES
How you can prevent, delay, even reverse Alzheimer’s Disease
