27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Among patients with probable Alzheimer disease and agitation who were receiving psychosocial intervention, the addition of citalopram compared with placebo significantly reduced agitation and caregiver distress; however, cognitive and cardiac adverse effects of citalopram may limit its practical application at the dosage of 30 mg per day. 5 key findings →
Participants: 186 Evidence: high
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Among persons with early Alzheimer's disease, the use of gantenerumab led to a lower amyloid plaque burden than placebo at 116 weeks but was not associated with slower clinical decline. 2 key findings →
Design: clinical trial Participants: 980 Evidence: low
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Elevated brain iron observed in AD has been associated with accelerated cognitive decline and may be a tractable drug target. 5 key findings →
Design: longitudinal study Participants: 167 Evidence: high
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Citalopram is effective in treating agitation in Alzheimer's dementia (AD), but it is associated with cognitive and cardiac risks, likely due to its R-enantiomer. 5 key findings →
Design: phase-3-trial Participants: 173 Evidence: null result
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Of 200 participants, 99 were assigned to methylphenidate and 101 to placebo. 5 key findings →
Design: longitudinal study Participants: 200 Evidence: high
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Patients with severe AD demonstrated greater efficacy compared to placebo on measures of cognition and global function. 3 key findings →
Participants: 176 Evidence: high
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Deep brain stimulation (DBS) is used to modulate the activity of dysfunctional brain circuits. 4 key findings →
Design: post-hoc analysis Participants: 42 Evidence: high
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When compared with propofol, dexmedetomidine sedation reduced incidence, delayed onset, and shortened duration of POD in elderly patients after cardiac surgery. 3 key findings →
Design: randomized controlled trial Evidence: high
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Although epidemiological and biochemical evidence suggests that aluminium may be associated with Alzheimer's disease (AD), there is no convincing proof of a causal link for aluminium in disease progression. 4 key findings →
Participants: 48 Evidence: low
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Donepezil and antidepressant therapy temporarily improved global cognition (treatment × time interaction, F₂,₂₁₆ = 3.78; P = .03), but effect sizes were small (Cohen d = 0.27, group difference at 1 year). 2 key findings →
Participants: 73 Evidence: high
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Although antipsychotics were associated with greater harm than antidepressants and anticonvulsants in subgroups of persons with dementia, medications used in lieu of antipsychotics for treating neuropsychiatric symptoms in dementia, such as anticonvulsants and dextromethorphan-quinidine, were also associated with harm. 5 key findings →
Design: randomized controlled trial Participants: 209 Evidence: high
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The amyloid-beta peptide Abeta(42) has been implicated in the pathogenesis of Alzheimer's disease (AD). 4 key findings →
Participants: 69 Evidence: low
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In a recent crossover trial, methylphenidate treatment decreased apathy in Alzheimer's disease. 4 key findings →
Participants: 37 Evidence: high
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No statistical difference was found in the efficacy of citalopram and risperidone for the treatment of either agitation or psychotic symptoms in patients with dementia. 5 key findings →
Participants: 103 Evidence: high
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Apathy is a common behavioral symptom of Alzheimer's disease (AD), being present in up to 70% of patients. 4 key findings →
Evidence: high
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The design decisions made for ADMET are important elements to be considered in trials assessing the safety and efficacy of medications for clinically significant apathy in Alzheimer disease. 1 key finding →
Evidence: high
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In the intention-to-treat analysis, dementia risk was not different between GLP1-RA and DPP4i initiators (hazard ratio [HR] 0.95, 95% confidence interval [CI] 0.87–1.04; rates: 6.29 versus 6.64 per 1000 person-years; mean follow-up: 6.54 years); however, continuous GLP1-RA versus DPP4i use was associated with a 21% lower risk (HR 0.79, 95% CI 0.64–0.97; rates: 3.64 versus 4.82; mean follow-up: 2.71 years). 4 key findings →
Design: cohort Participants: 107,424 Evidence: moderate
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The effects of antidepressants on mood, cognition and the daily activities of Alzheimer patients are ambiguous. 1 key finding →
Evidence: high
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Mean (SD) β-glucocerebrosidase levels were higher at week 26 (ambroxol, 12.45 [1.97] nmol/h/mg; 91% CI, 11.54-13.36 nmol/h/mg); placebo, 8.50 [1.96] nmol/h/mg; 91% CI, 7.65-9.34 nmol/h/mg; P = .05) in the ambroxol group compared with placebo. 3 key findings →
Design: clinical trial Participants: 75 Evidence: high
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Our results support the positive cognitive effects of boswellic acids by reducing the systemic inflammation. 5 key findings →
Design: randomized controlled trial Evidence: high
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Donepezil was relatively well tolerated; adverse events were consistent with current labeling. 2 key findings →
Participants: 974 Evidence: high
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The purpose of this study was to investigate the effects of a walking/talking program on residents' communication, ambulation, and level of function when there were two residents to one care provider (2:1). 2 key findings →
Evidence: high
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Additional study of mechanisms of action and methods for titrating stimulation parameters will be needed to determine if DBS has potential as an AD treatment. 2 key findings →
Design: post-hoc analysis Participants: 42 Evidence: high
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Treatment outcomes in CitAD showed modest, although statistically significant, influence of genetic variation at HTR2A and HTR2C loci. 3 key findings →
Evidence: high
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This study aimed to identify lipid species associated with MPH response and explore lipid pathway disruptions in responders versus non-responders. 3 key findings →
Design: randomized controlled trial Evidence: low
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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
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.
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.
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 →