27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Alzheimers disease (AD) is characterized by substantial clinical and biological heterogeneity, with diverse neuroanatomical, cognitive, clinical, functional, and genetic risk profiles that are poorly captured by current diagnostic frameworks. 4 key findings →
Participants: 393 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
BACKGROUNDSubjective cognitive decline (SCD) may precede mild cognitive impairment (MCI), but not all individuals with SCD progress to MCI. 5 key findings →
Design: longitudinal study Participants: 1,352 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
BackgroundDeep-learning models predict mild cognitive impairment (MCI)-to-Alzheimers disease (AD) conversion from structural MRI with high accuracy. 1 key finding →
Design: longitudinal study Participants: 40 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
BackgroundNon-pharmacological interventions may enhance motor-cognitive integration in prodromal Alzheimers disease (pAD). 5 key findings →
Design: randomized controlled trial Participants: 68 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
ObjectivesSubjective word-finding complaints (SWFC) are among the most frequent cognitive complaints in cognitively unimpaired older adults (CU). 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
--Clinical trajectories after a diagnosis of mild cognitive impairment (MCI) vary widely, so prognostic models must account for both the timing of subsequent diagnoses and unequal follow-up. 2 key findings →
Participants: 401 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
IntroductionRemote cognitive assessments offer an accessible, scalable way to support clinical characterization and longitudinal monitoring of cognition. 3 key findings →
Design: longitudinal study Participants: 209 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
INTRODUCTIONDetermining whether plasma biomarkers are preferentially associated with Alzheimers disease (AD)-related rather than age-related brain atrophy patterns may clarify their prognostic and diagnostic clinical use. 5 key findings →
Design: cross-sectional Participants: 818 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Subjective cognitive decline (SCD), the self-reported experience of worsening or more frequent memory loss or confusion, might be a symptom of early-stage dementia or future serious cognitive decline such as Alzheimer disease* or a related dementia (ADRD) (1). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) pathology accumulates years before overt cognitive impairment, yet its multidomain phenotype remains poorly defined. 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Impaired peripheral clearance of amyloid-β (Aβ) contributes to Alzheimer's disease (AD) pathogenesis. 2 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
These findings support MRI-derived LC intensity as a marker of early AD-related processes and suggest that LC intensity may provide complementary information not captured by plasma pTau 217 alone. 4 key findings →
Design: longitudinal study Participants: 163 Evidence: moderate
Full summary, score breakdown and related studies → Original source
These data further support the use of the LOAD2.Mthfr 677C>T mouse model to study aspects of ADRD such as cerebrovascular compromise. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid-β and tau, pathological hallmarks of AD, silently accumulate years before clinical symptoms’ onset and are associated with neuronal dysfunction and cognitive impairment. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
As the world's population ages, Alzheimer's disease (AD), a progressive neurodegenerative disorder, is becoming more common. 1 key finding →
Participants: 59 Evidence: low
Full summary, score breakdown and related studies → Original source
Residualized WMH T1w/T2w-FLAIR ratio captures lesion-specific microstructural variation missed by volumetric measures, consistent with vascular-gliotic injury in VD and coexisting amyloid-linked demyelination in AD. 4 key findings →
Design: cross-sectional Participants: 71 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Neuropsychiatric symptoms (NPS) are highly prevalent in Mild Cognitive Impairment (MCI), conceptualized as an intermediate clinical state between normal aging and dementia. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
The basal forebrain is an early site of pathology in Alzheimer’s disease (AD). 3 key findings →
Design: longitudinal study Participants: 116 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) pathology is increasingly recognized to manifest in the retina, offering a non-invasive window for early biomarker discovery. 2 key findings →
Design: longitudinal study Participants: 40 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Four distinct subtypes were identified: I low-risk healthy aging, II behavioral/social vulnerability, III cardiometabolic–depressive multimorbidity, and IV mixed social-medical vulnerability profiles. 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Individuals who carry two copies of the apolipoprotein E ε4 ( APOE ε4) allele are at high risk of developing Alzheimer’s disease (AD), yet the effects of APOE ε4 homozygosity on biological pathways related to AD over the lifespan are unknown. 1 key finding →
Participants: 413 Evidence: low
Full summary, score breakdown and related studies → Original source
This provides the first evidence in older adults with cognitive concerns that higher step counts are associated with fewer depressive but more anxiety symptoms. 5 key findings →
Design: randomized controlled trial Participants: 629 Evidence: high
Full summary, score breakdown and related studies → Original source
In a recent open-label, single-arm study, vortioxetine, an antidepressant, was associated with improved cognitive function in patients with MCI, however, no placebo-controlled studies have been conducted to support these findings. 5 key findings →
Design: randomized controlled trial Evidence: high
Full summary, score breakdown and related studies → Original source
Individuals diagnosed with mild cognitive impairment (MCI) have an increased risk of developing dementia. 1 key finding →
Participants: 100 Evidence: high
Full summary, score breakdown and related studies → Original source
Wearable devices repeatedly measure activity, sleep, and nocturnal physiology, but their value for three-class cognitive screening remains uncertain. 1 key finding →
Participants: 174 Evidence: low
Full summary, score breakdown and related studies → Original source
10 of the 2,090 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
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 →