27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Targeted clinical application of specific technologies is poised to revolutionize precision care in dementia as these technologies may be used both by patients and caregivers, and at a systems level to provide safe and effective care. 2 key findings →
Design: systematic review Participants: 1,337 Evidence: high
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Accumulating evidence demonstrates that metabolic changes in the brain associated with neuroinflammation, oxidative stress, and mitochondrial dysfunction play an important role in the pathophysiology of mild cognitive impairment (MCI) and Alzheimer's disease (AD). 4 key findings →
Design: meta-analysis Evidence: high
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TRIAL REGISTRATION clinicaltrials.gov Identifier: NCT00257712. 1 key finding →
Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
In the new AA diagnostic criteria, AD can be defined clinically as encompassing cognitively normal people having a core 1 AD biomarker. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The majority of participants were female and were taking concomitant psychotropic medications (antidepressants and antipsychotics) at baseline. 3 key findings →
Design: phase-2-trial Participants: 75 Evidence: early
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Two hundred eighty dyads were enrolled. Caregivers during the intervention period reported lower levels of RSS of 0.7 points (standard deviation [SD]: 0.8) compared to the caregivers in the control period. 5 key findings →
Design: randomized controlled trial Evidence: high
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Validation of the safety and efficacy of ECT in patients with advanced AD with refractory agitation and aggression is necessary. 5 key findings →
Design: randomized controlled trial Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
The epsilon2 allele confers a protective effect, and women with DS have an increased risk for AD, as in the general population. 5 key findings →
Participants: 57 Evidence: moderate
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These findings suggest that at current expected prices, neither aducanumab nor donanemab would be cost-effective for early AD in the US. 2 key findings →
Design: clinical trial Evidence: low
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Patients with AD and patients with FTD show different disturbances in their rhythms of activity and temperature compared with each other and with normal elderly patients. 3 key findings →
Participants: 23 Evidence: moderate
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Epidemiological evidence suggests that the incidence of amyotrophic lateral sclerosis is increased in association with head injury. 5 key findings →
Evidence: low
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The relationship between progressive cognitive decline and underlying neuropathology associated with Alzheimer s disease (AD) is a key issue in defining the mechanisms responsible for functional loss. 4 key findings →
Participants: 20 Evidence: low
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The early endosome is the first vacuolar compartment along the endocytic pathway. 5 key findings →
Evidence: low
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The activity of the pyruvate dehydrogenase complex (PDHC) was reduced in affected areas of brain from patients with Huntington disease (caudate, putamen) and Alzheimer disease (frontal cortex) where choline acetyltransferase (CAT) activity was low. 1 key finding →
Evidence: low
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Calcium-activated neutral proteinases (CANPs or calpains) are believed to be key enzymes in intracellular signaling cascades and potential mediators of calcium-induced neuronal degeneration. 4 key findings →
Participants: 22 Evidence: low
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Affective symptoms are of prognostic utility, but interventions to prevent dementia syndromes are limited. 1 key finding →
Evidence: low
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Type 2 diabetes mellitus (T2DM) is a risk factor for Alzheimer disease (AD). 2 key findings →
Evidence: low
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Endocytic dysfunction is an early pathological change in Alzheimer's disease (AD) and Down's syndrome (DS). 3 key findings →
Evidence: low
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A decline in instrumental activities of daily living (IADL) correlates with the progression from mild cognitive impairment (MCI) to Alzheimer's disease (AD) dementia and has been associated with frontal and parietal hypometabolism, lower cerebrospinal fluid amyloid β 1-42 , and inferior temporal cortical thinning. 4 key findings →
Design: cross-sectional Evidence: low
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Sleep disruption and other circadian rhythm disturbances are frequently seen in dementia patients. 2 key findings →
Participants: 30 Evidence: low
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These data support the hypothesis that neuronal endosomal dysfunction is associated with preclinical AD. 4 key findings →
Evidence: low
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Understanding the mechanisms of amyloid-beta protein (Abeta) production and clearance in the brain has been essential to elucidating the etiology of Alzheimer disease (AD). 4 key findings →
Evidence: low
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The formation of beta-amyloid in the brains of individuals with Alzheimer disease requires the proteolytic cleavage of a membrane-associated precursor protein. 4 key findings →
Evidence: low
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Calbindin-D28k (CB), one of the major calcium-binding and buffering proteins, has a critical role in preventing a neuronal death as well as maintaining calcium homeostasis. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Adults with Down syndrome (DS) have an exceptionally high frequency of Alzheimer disease (AD) with a wide variability in onset, from 40 to 70 years of age. 2 key findings →
Participants: 232 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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 →