> Early detection of Alzheimer’s disease is important since the first treatments capable of slowing the progression of the neurodegenerative disease recently became available to patients, and these drugs are more effective when started sooner rather than later. Other promising investigational drugs are in the pipeline.
A very good friend's wife had Alzheimer's caught early, and the medication she's on stopped its progression. It's much better for her than my family members who had no treatment options.
It’s also not clear that one can measure progression well enough that an n=1 data point is meaningful. And I’m also far from convinced that very early Alzheimer’s that would progress rapidly enough to be noticeable can be detected with enough specificity to rule out fairly common cases of people who test positive but effectively don’t have the disease.
Best wishes to your friend’s wife.
He has taken a personal interest in preventing dementia and wants to take the first generation Alzheimer’s drugs, specifically leqembi that works on amyloid plaques. And this is definitely a tough choice, because eventhough it does show some slowing of the disease, it has lot of side effects that may not be worth it.
Personally, I am against it and don’t think it’s worth it as he could do permanent damage to himself. Think he should hang on until the second generation of drugs come out, which should be in the next 1-3 years (there a lot of Alz drugs in the pipeline, but you never know of course if anything will pan out). It’s a tough choice and don’t know if there is a good option at this point.
Google scholar link for the article https://scholar.google.com/scholar?cluster=10296105574478709...
What a time to be alive
what medication is that?
But hopefully we'll start to have more options and wider approvals for things like anti-amyloid drugs.
Isn’t the viewpoint in the last decade that amyloid plaques are likely a finding rather than the underlying cause of Alzheimer’s Disease?
Those in it are still throwing billions per year at the idea.
Meanwhile, back in reality, no amyloid-beta drug has had any clinical effect in humans, other than reducing the plaques. But both the shingles and RSV vaccines are proven to reduce Alzheimer's risk.
I can't think of a good reason why this happened.
[0] https://www.npr.org/2021/06/11/1005567149/3-experts-have-res...
It's (almost) purely determined by genetics. You can't do anything to improve it, other than to improve every other cardiac related risk factor.
(There are some experimental drugs in the pipeline, though)
The only other alternative is some sort of mental hospital which is more like a prison than anything else.
If you do go into long-term care, Medicaid will probably seize your assets to help pay for everything. For example, a house in your name. They'll use those to pay back what they paid for your care.
So if you're gonna get sick and you're gonna be a burden in your old age, best to plan for leaving this world the way you came in: naked and penniless.
>>Mutations in PSEN1 and APP are associated with complete penetrance, meaning that all individuals who have a PSEN1 or APP mutation will develop AD if they live a normal lifespan [1]
and
>>[Age-of-onset] Usually 40s or early 50s (range 30s-early 60s) [2]
Note that this is only for early-onset Alzheimer's, representing ~5% of all Alzheimer's.
>>Our study showed that the rate of EOAD in AD is 5.5%, not 1-2% as usually demonstrated. And our results indicated that the rate in developed countries was relative higher than in developing countries [3]
[1]https://pmc.ncbi.nlm.nih.gov/articles/PMC3326653/
[2]https://www.ncbi.nlm.nih.gov/books/NBK1161/table/alzheimer.T...
I've seen up close what dying with these kinds of illnesses look like. For me, a positive test would be a sign that it may be time to say my goodbyes and plan my exit.
Given the widely-reported extent of p-hacking in the biomedical literature over the decades, I’m surprised anyone would float an avid ‘but how could research scientists ever be wrong’ default reflex.