Talk:Alzheimer's disease

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Most cases ARE familial

The citation provided for the comment “most cases are not familial” demonstrates the exact opposite of what this article claims it does. Urbansiberia (talk) 04:01, 30 October 2025 (UTC)

  • Greetings Wikipedians! My neurologist tells me that patients with two copies of the e4 gene (e4/e4) are 8 to 12 times more likely to develop AD. This article supports that: What APOE Means for Your Health. I will leave it to someone more expert to decide how to edit the Wikipedia article. Cordially, BuzzWeiser196 (talk) 14:28, 27 January 2026 (UTC)
    Only a small minority of Alzheimer’s disease (AD) cases are truly familial in the strict, Mendelian sense. Therefore, one can understand why some Wikipedians would dispute the claim that most cases of AD are familial, or at least argue that it is misleading.
    “Familial AD” is usually reserved by geneticists for cases caused by autosomal‑dominant mutations (APP, PSEN1, PSEN2). These monogenic forms account for 1-5% of all cases. That said, “having a family history of AD” is much more common and reflects shared polygenic risk (for example APOE E4) plus environment, not a single causative "Mendelian" mutation. Therefore AD does tend to "run in families" which a lay writer might consider synonymous for "familial". First‑degree relatives of a person with AD have roughly a 2–3‑fold increased lifetime risk compared with the general population, reflecting substantial but complex heritability. APOE4 confers risk for both sporadic and late‑onset familial AD but does not follow simple high-penetrant Mendelian inheritance. Many patients report another affected family member, so “familial aggregation” is common even when no autosomal‑dominant pattern is present. So in short, if “familial” is used loosely to mean “often runs in families,” then one might claim that concept for many or most cases of AD, but that is different from saying they are 'familial' in the strict genetic sense.
    A rewrite of the article could avoid the term "familial" completely, as it is confusing, ambiguous, and/or interpreted differently by different readers. Maybe with text like: "Most AD cases are sporadic and lack an identifiable single‑gene cause, although they are influenced by polygenic (including APOE influence) and environmental risk factors and frequently cluster in families. Only a small minority of cases represent autosomal‑dominant AD caused by highly penetrant mutations in APP, PSEN1, or PSEN2." Jaredroach (talk) 15:13, 27 January 2026 (UTC)

No mention of disease-modifying anti-amyloid drugs (i.e. Leqembi & Kisunla)

Leqembi and Kisunla are noted as the first FDA-approved "disease-modifying" treatments for Alzheimer's, so-called as they modify the trajectory of Alzheimer's by removing amyloid plaque. The current Wikipedia entry for Alzheimer's states that "No treatments can stop or reverse its progression, though some may temporarily improve symptoms." Leqembi & Kisunla do not "temporarily improve symptoms", they are disease-modifying treatments as they impact the trajectory of Alzheimer's. DMcKissock (talk) 23:05, 16 November 2025 (UTC)

These are brand names for the drugs lecanemab and donanemab that are referred on page Iztwoz (talk) 09:50, 25 January 2026 (UTC)
I agree. But I still contend the overall tone of the wikipedia article is not current. I previously quoted the factually incorrect statment on the page that "No treatments can stop or reverse its progression, though some may temporarily improve symptoms." Lecanemab and Donanemab do *not* treat symptoms, rather they remove amyloid plaque. The references to Lecanemab & Donanemab on the Wikipedia page are in the section "Management" which begins with "Thre is no cure for AD, available treatments offer relatively snmall symptomatic benefits but remain pallative in nature." Again, another factually incorrect statement. As reported in the Donanemab Appropriate Use Recommendations (availble for free on the web), the Phase 3 trial with Donanemab resulted in 29.7% of the participants receiving the active drug being amyloid clear at 6 months, 66% at 1 year, and76.4% at 18 months. This is not pallative, but rather the amyloid removal is changing the trajectory of the disease.
At the Alzheimer's Association International Conference (AAIC) in Toronto in July 2025, Eisai presented results from real-world experience with Lecanemab, showing similar ARIA rates as in the clinical trials (one of the concerns was that real-world experience might have higher ARIA rates).
At the recent Clinical Trials on Alzheimer's Disease (CTAD) conference in San Diego, Eisai presented information on their estimates of the 10-year time-savings benefits of Lecanemab treatment. They estimated that ongoing Lecanemab treatments started after a mild cognitive impairment diagnsosis of Alzheimer's may delay disease progression to mild dementia by 2.5 years, and a delay to moderate dementia by 3.5 years. Further, for those who had mild cognitive impairment and started treatment with low amyloid levels, Lecanemab worked better and would delay progression to mild dementia by 6 years and moderate dementia by 8.3 years. ~2026-53959-4 (talk) 16:44, 25 January 2026 (UTC)
What is stopping you from making the changes yourself? Iztwoz (talk) 17:04, 25 January 2026 (UTC)
I guess nothing ?!? I've used Wikipedia but never before made a change. ~2026-53959-4 (talk) 19:22, 25 January 2026 (UTC)
Go for it - it's a worthwhile pastime Iztwoz (talk) 10:37, 26 January 2026 (UTC)

Gut-brain axis and dietary mitigation info

Hi! I am doing some reading about diet’s role in AD mitigation and have come across some recent reviews highlighting the role of nutrition and the microbiota-gut-brain axis in mechanistic prevention. These highlight that gut dysbiosis leads to key pathological features of AD like blood-brain barrier dysfunction, overactive microglia, excessive pro-inflammatory cytokines, and endotoxin induced increase of Aβ.

In the current article, the Disease mechanism subsection of Pathophysiology presents much concerning the link between immune function and neuronal disease progression. Despite this, no connection is made to the gut-brain axis mitigation of this. I think the sources presented could warrant an addition about gut-brain interplay under Disease mechanism.

Even if not, I might also suggest a reconsideration of whether Management is truly the best place to incorporate existing info on diet. It seems diet could instead (or additionally) be incorporated into the Lifestyle subsection of Prevention with exercise, even when considering the existing material cited (source 269). I understand the ambiguity of prevention versus management considering that the disease's progression is so gradual, but I’d appreciate your thought on the matter.

Thank you! Alpaca974 (talk) 17:27, 8 December 2025 (UTC)

Both sources you offer contain only conjecture from lab research. The MDPI-Nutrients publication is unreliable as a predatory source, while the AJP ref only speculates from lab studies about an unproved gut-brain mechanism in AD pathogenesis.
WP:MEDASSESS - no health technology assessment, clinical guideline on a preventative AD dietary plan, or reputable review acknowledges significance of this putative axis in AD onset. Zefr (talk) 17:48, 8 December 2025 (UTC)
Probably the phrase "gut-brain axis" is a bit esoteric to be included in a high-level Wikipedia article on AD. It might be undefined, or poorly defined, or unproven, or controversial, etc. However do not get distracted by this term. Do not dismiss "diet" if dismissing "gut-brain axis". Diet is exceptionally important in preventing and treating AD. The article must emphasize diet if it discusses prevention and treatment. Jaredroach (talk) 15:51, 27 January 2026 (UTC)

Improving top-importance medicine articles: Join the Vital Signs campaign 2026

The goal of the Wikipedia:WikiProject Medicine/Vital Signs 2026 campaign is to bring all 101 top-importance articles—including this one—up to at least B-class quality. Many of these articles are widely read but overdue for review, so even small improvements can have a big impact.

If you watch or edit this article, your help would be very welcome. You can:

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To reach B class, articles should have: suitable referencing, reasonable coverage, a clear structure, good prose, helpful illustrations, and be understandable to a broad audience. Contributions of any size are appreciated. Femke (talk) 16:00, 20 December 2025 (UTC)

Lithium and AD

I agree that the Li/ AD connection is preliminary. However, the general Wikipedia reading public need to be informed. The research includes both chemical, biochemical, human and animal results, not just animal tests. For that reason, this research has been discussed in notable scientific journals and by US Federal websites (NIH). Note I make no claim about the value of Li supplements, just reporting important research, which is factual. It is worthwhile considering that negative results on AD treatments ARE in the article and have not been ruled outside the scope. Zeamays (talk) 18:03, 9 January 2026 (UTC)

Especially for a topic like AD, we do not discuss early-stage lab research as if it has encyclopedic relevance, WP:MEDASSESS, bottom of left pyramid, WP:IN MICE. The encyclopedia is not intended for news announcements, WP:NOTNEWS. Zefr (talk) 18:37, 9 January 2026 (UTC)
Why do you allow failed treatments to be discussed then? Zeamays (talk) 19:09, 9 January 2026 (UTC)
Sources in the article are reputable clinical guidelines, systematic reviews or Cochrane reviews, having been well-vetted over years. The lithium orotate research involving biopsies, mice studies, and in vitro analysis is at the earliest stage of treatment assessment, many years away from confirmation as a promising agent. Zefr (talk) 21:25, 9 January 2026 (UTC)
Predicting the future is not a worthy argument. Zeamays (talk) 14:30, 18 January 2026 (UTC)
If overview sources (like narrative reviews about Alzheimer's) discuss it extensively in their research outlook sections, we could discuss it too. That usually doesn't happen with early research however. —Femke 🐦 (talk) 18:29, 18 January 2026 (UTC)
This article (and other supporting papers) have been reviewed extensively in premier publications and web sites, including Science, Harvard Medical School News & Events, the NIH, and the American Psychiatric Association (APA)'s Psychiatry Online. I can easily cite others. --Zeamays (talk) 15:36, 22 January 2026 (UTC)
These are all non-peer reviewed sources based on primary research, which do not meet the strict requirements of WP:MEDRS. What we need is a review paper that came out recently and see if they discuss the finding. A lot of research about dementia comes out every week, so we need to figure out if it's WP:DUE to talk about this particular bit of knowledge. With research in mice, the answer is usually no, unless it's mentioned extensively in overview sources (a source that is about all aspects of Alzheimers). —Femke 🐦 (talk) 17:32, 22 January 2026 (UTC)
It is unfair to expect that peer-reviewed reviews would already have been published to have already considered such new results. One must consider the premier quality of the reviews that have already been published to review the Nature paper. I also think you are treating AD research unfairly in comparison to other laboratory research on metabolic diseases. There is a range of quality in original published research, and the strict editorial standards of Nature are well-recognized in the research community. Zeamays (talk) 20:30, 22 January 2026 (UTC)
Nature is known for publishing the newest and most high impact research. Which means a lot of major scientific breakthroughs are reported first in that journal. But it has a flip-side as well: the newer and more ground-breaking your research is, the more likely you've made some mistake. Nobody has tried what you've done, you're treading on new ground. There is for instance some research indicating that non-reproducable research is cited more. Some indices of reliability are less robust in higher-impact journals.
WP:MEDRS sometimes allows primary research, but that is usually only for big trials that are almost guaranteed to be described in a secondary source within the year. WP:MEDPRI explains that a lot of pre-clinical research is not reproducible.
And it might be that other diseases on Wikipedia do use these sources. They should not either, but Wikipedia is a work in progress, so perhaps we can replace those statements with more recent reviews. —Femke 🐦 (talk) 20:51, 22 January 2026 (UTC)
That said: there is a single that discusses it: https://www.sciencedirect.com/science/article/pii/S1568163724000217?via%3Dihub. The number of human participants so far is 89, a very low number. I've had a look at the first 3 overview sources that mention therapy on PubMed and it does not seem to be mentioned once in any of them: , , ? —Femke 🐦 (talk) 21:04, 22 January 2026 (UTC)
It is wrong not to put new research results in Wikipedia. Excluding contemporary research gives the false impression that there is no activity in Alzheimer's disease. You are wrong about erroneous results, Wikipedia is a living document (haven't you noticed?) where errors are quickly corrected. Zeamays (talk) 16:53, 25 January 2026 (UTC)
Please also see the archived Discussion we had on this a few months ago.
Talk:Alzheimer's disease/Archive 13#c-Jaredroach-20250812185800-Tillman-20250807143700 Jaredroach (talk) 14:43, 23 January 2026 (UTC)