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Find studies

Showing 1,226–1,250 of 1,489 studies in Treatments (page 50 of 60) · 27,380 in the whole library · How the 0–100 score works

Browse by subject, author or institution

Each number is how many studies that link shows, with your other filters kept.

What “Treatments” covers

Treatments — Drug and non-drug treatment research — what was tested, in whom, and what changed — plus the approvals and coverage decisions that followed.

A note on reading research. One study is rarely the final word.

We try to note the size of a study, whether it was in humans or animals, and how early-stage the finding is. If a summary here doesn't make that clear, treat it with extra caution and check the original source.

36% of practitioners reported not having used therapies for medical conditions other than dementia in patients with AD for reasons of limited compliance in these patients. 5 key findings →

Evidence: low

The combination of memantine, an N-methyl-d-aspartate (NMDA) receptor antagonist, with an acetylcholinesterase inhibitor (AChEI) is the current standard of care in Alzheimer's disease (AD). 2 key findings →

Evidence: low

Cerebrovascular disease (CVD), as well as secondary ischemic brain injury from cardiovascular disease, are common causes of dementia and cognitive decline in the elderly. 1 key finding →

Evidence: low

The management of dementia in Alzheimer's disease has dramatically changed since the development of anti-dementia drugs. 5 key findings →

Evidence: low

Based on efficacy and safety data, several drugs have been approved for symptomatic improvement of dementia of the Alzheimer type and one for the symptomatic improvement of dementia associated with Parkinson's disease. 4 key findings →

Evidence: high

These studies have shown that PPF 300 mg t.i.d. is safe and well tolerated when taken on an empty stomach 1 h before meals. 5 key findings →

Evidence: high

The intervention in the Digital, Cognitive, Multi-domain Alzheimer Risk Velocity is uniquely designed to reduce the risk of AD through a web-based health coaching experience that addresses the modifiable lifestyle-based risk factors. 3 key findings →

Evidence: low

Improvements in the aspects evaluated are expected in the IG compared to CG. 1 key finding →

Evidence: high

Lecanemab use for early Alzheimer disease in Canada

✓ Peer-reviewed alzhub usefulness score 37 out of 100. Canadian Medical Association Journal 2026-06-28

Lecanemab is a humanized monoclonal antibody that binds soluble brain amyloid-β protein, promoting its removal and slowing the underlying process of Alzheimer disease. 1 This mechanism aligns with the amyloid hypothesis, a debated model of Alzheimer disease pathogenesis.1 Only patients with mild cognitive impairment (MCI) or mild dementia due to Alzheimer disease are eligible for lecanemab treatment. 1 key finding →

Evidence: low

The authors of this mini-review list the key benefits (e.g., positive results of the reviewed randomized clinical trials studies for the improvement of cognitive decline in AD) and limitations (e.g., low awareness of benefits of TCM in Europe) of Chinese medicine therapy for the treatment of AD. 2 key findings →

Evidence: high

Within the limitations of measuring in vitro equilibrium binding activity of in‐house recombinant antibodies to aqueously extracted Aβ from human postmortem brain tissue, we could not discern a population of Aβ aggregates ( e.g . protofibrils) accessible to one antibody but not the other two. 3 key findings →

Evidence: low

The anti-amyloid monoclonal antibody lecanemab received the US accelerated approval for mild cognitive impairment or mild dementia stage of Alzheimer disease in January 2023, which was converted into traditional approval in June 2023. 5 key findings →

Evidence: low

Our results show that lecanemab exhibits high binding affinity to amyloid-β fibril structures that have a flexible N-terminus in common, as is the case for type I, type II and murine type III amyloid-β fibril polymorphs, which resemble or are identical to human structures observed in sporadic and familial cases of Alzheimer's disease, including a case with the Arctic (E22G) mutation. 5 key findings →

Evidence: low

Lecanemab reduced clinical decline by roughly 27% over placebo, with ARIA-E in 12.6% of treated patients;donanemab slowed decline by about 35%, with ARIA-E near 24%. 4 key findings →

Design: narrative review Evidence: high

Alzheimer's disease (AD) affects ~55 million people globally and is projected to rise steeply with population ageing. 1 key finding →

Design: longitudinal study Evidence: moderate

TDP-43 proteinopathies encompass frontotemporal lobar degeneration with TDP-43 pathology (FTLD-TDP), amyotrophic lateral sclerosis (ALS-TDP), and limbic predominant age related TDP-43 encephalopathy neuropathological change (LATE-NC). 3 key findings →

Evidence: moderate

Die amyloide Selbstassemblierung von α‐Synuclein (αSyn) wird mit der Pathogenese der Parkinson‐Krankheit (PD) in Verbindung gebracht. 5 key findings →

Evidence: low

Two approaches--molecular cloning and immunochemical analysis--have identified one of the components of Alzheimer's disease amyloid deposits as the serine protease inhibitor alpha 1-antichymotrypsin. 1 key finding →

Evidence: low

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Where “Free full text” comes from

Free full text links and the Full text may need a subscription label come from Unpaywall, Europe PMC and OpenAlex records of free copies, checked 10 Oct 2026. A study with neither is unknown, not paywalled. Show only studies that are free to read

How the 0–100 score works — and why some entries are capped

This is alzhub's own score. It is not an official metric, not an impact factor, and no journal, publisher or ranking body endorses it. We built it so that a reader who is not a scientist can tell a landmark trial from a conference abstract without having to already know the difference. Every point comes from one of 20 components, all of them printed on the study itself, so you can disagree with our arithmetic rather than having to trust the total.

  • Journal tier up to 10 pts
  • Journal's citation record up to 4 pts
  • Study design up to 12 pts
  • Strength of evidence up to 5 pts
  • Peer-review validation up to 10 pts
  • How recent up to 5 pts
  • Sample size up to 4 pts
  • Effect reported up to 3 pts
  • Studied in people up to 3 pts
  • Randomised / blinded up to 2 pts
  • Times cited up to 7 pts
  • Citations per year up to 5 pts
  • Impact for its field and year up to 6 pts
  • Cited by studies here up to 6 pts
  • Still being cited up to 4 pts
  • Senior author's track record up to 4 pts
  • Institution's track record up to 3 pts
  • Multi-centre collaboration up to 3 pts
  • Indexed in PubMed up to 2 pts
  • Free to read up to 2 pts

Journals are placed in ordered tiers, never given a numeric impact factor — we could not verify current impact factors from a source we control, and an invented one would be worse than none. Tier 1 is the top-tier general journals (NEJM, The Lancet, JAMA, Nature, Science, Nature Medicine); tier 2 is the leading specialty journals; tier 3 is every other peer-reviewed journal. A separate part scores how much the journal's own papers are cited, which tells the tier-3 journals apart.

Two rules we don't bend. First, we never fill in a missing value: if a record does not state a sample size or a design, that component scores zero, and if we simply have no data for a part, such as a citation count, that part is left out and the study is scored on the parts we could check. The study card says which. Second, anything that is not a peer-reviewed article is capped at 16/100 and carries a warning chip — so a conference abstract or a company press release can never outrank a peer-reviewed paper, no matter how good it looks.

We rank a rigorous null result — a good trial showing that something does not work — above an early positive finding. Someone deciding whether to buy a supplement is served by that, and the rigour is already counted by the design and journal components.

The score is computed from the published data alone and is reproducible: the same file always yields the same numbers.

See the whole rubric drawn out → — four charts covering all 27,380 studies: how the scores are spread and where the cap bites, which of the 20 components the library is strong and weak on, which subjects rest on stronger evidence, and what kinds of study each subject is actually built from.

What this library is — and isn't

This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), plus smaller pulls from PubMed, Crossref and medRxiv. If a study, a drug, or a finding isn't here, that is not evidence it doesn't exist in the literature — it may simply not have been pulled in yet.

1,032 records (3.8% of the library) are not peer-reviewed — 962 of those are preprints posted before any journal review, and the rest are conference abstracts, regulatory notices and reports. Every study card on this page states its status plainly, and the score above is capped for anything that isn't a peer-reviewed article.

See the full, machine-readable breakdown of this library's coverage →

Newest studies, as a dated timeline →    Atom feed