As of October 2025, we have recruited 200 participants. 4 key findings →
Participants: 200 Evidence: high
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27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
As of October 2025, we have recruited 200 participants. 4 key findings →
Participants: 200 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Among 6303 hospitalized patients with ADRD, 39.3% had mild dementia, 57.8% moderate, and 2.9% severe. 5 key findings →
Evidence: moderate
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There were 361 deaths. Median survival was longer for residents with advanced dementia and frailty (16.5 months, 95%CI:13.5–19.5 months, P < 0.001) compared to incurable cancer (8.1 months, 95%CI:5.1–11.1 months, P < 0.001) and end-stage organ failure (7.7 months, 95%CI:3.0-12.4 months, P < 0.001). 5 key findings →
Design: cohort study Evidence: moderate
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< 0.1). -ε4 status, and Aβ load, and not mediated by markers of neuroaxonal degradation. 3 key findings →
Evidence: low
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White matter hyperintensities (WMH) are associated with cortical thinning in distant brain regions. 5 key findings →
Design: cross-sectional Participants: 551 Evidence: moderate
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Individuals with msWMH showed systematic deficits in face-memory processing across encoding, maintenance, and retrieval, accompanied by reduced theta power and synchronization, altered alpha power, and disrupted theta-gamma coupling. 5 key findings →
Design: longitudinal study Evidence: moderate
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Describe geographic variation from 2019 to 2023 in assisted living (AL) and memory care supply, and its correlation with county-level characteristics. 2 key findings →
Participants: 1,000 Evidence: low
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This study examines the difference in functional outcomes among Traditional Medicare (TM) and Medicare Advantage (MA) beneficiaries with Alzheimer’s disease and related dementias (ADRD) during a home health admission, which is unknown. 5 key findings →
Design: cohort study Participants: 81,735 Evidence: moderate
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Microglial activation is an early and common feature of almost all neuropathologies, including multiple sclerosis, Alzheimer's disease and mechanical injury.
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Gene therapy to treat hereditary disorders conventionally delivers the normal allele to compensate for loss-of-function mutations. 2 key findings →
Evidence: preliminary
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Medicare Part D drug spending was substantial, increasing with dual-eligibility duration: $8732-$9107 among beneficiaries with full-year dual eligibility and exceeding $11 500 among those with 5+ chronic conditions. 1 key finding →
Design: cross-sectional Participants: 1,372,696 Evidence: moderate
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Burden of chronic intravenous treatments exceed the gross medical and social care cost savings and value of caregiver benefit. 3 key findings →
Design: modelling Evidence: preliminary
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We previously reported that T96K is a gain-of-function mutation in TREM2 based on its ability to increase ligand-dependent activation. 3 key findings →
Evidence: early
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Alzheimer disease (AD) is the most prevalent neurodegenerative disorder leading to dementia in the elderly. 1 key finding →
Evidence: low
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Imbalance in production and clearance of amyloid beta (Aβ) is the primary reason for its deposition in Alzheimer disease. 4 key findings →
Evidence: low
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Currently, 3 amyloid PET tracers are approved and commercially available for clinical use. 2 key findings →
Evidence: low
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Glutamate transporter solute carrier family 1, member 2 (GLT1/EAAT2), a major modulator of glutamate homeostasis in astrocytes, is assessed in post-mortem human brain samples of frontal cortex area 8 in advanced stages of Alzheimer disease (AD) and terminal stages of dementia with Lewy bodies (DLB) in order to gain understanding of astrogliopathy in diseases manifested by dementia. 4 key findings →
Evidence: low
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Hyperphosphorylated tau protein deposits and, inflammatory processes are characteristic components of Alzheimer disease (AD) pathology. 5 key findings →
Evidence: low
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Glial fibrillary acidic protein (GFAP) is a well-established astrocytic biomarker for the diagnosis, monitoring and outcome prediction of traumatic brain injury (TBI). 4 key findings →
Evidence: low
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Clinical trials to advance the diagnosis and treatment of Alzheimer disease (AD) may expose research subjects to discrimination risks. 3 key findings →
Evidence: low
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Quantification results using the proposed deep learning-based method showed stronger correlations with the FreeSurfer estimates than SPM-based SN using MRI did. 5 key findings →
Evidence: low
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Recent functional magnetic resonance imaging studies have demonstrated that moment-to-moment variability in the blood oxygen level-dependent (BOLD) signal is related to age differences, cognition, and symptomatic Alzheimer's disease (AD). 1 key finding →
Participants: 321 Evidence: low
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Brain 18F-FDG PET scans interpreted with Neurostat and 3D-SSP displays accurately detected Alzheimer disease in patients with primary progressive aphasia or corticobasal syndrome as focal-onset dementias. 2 key findings →
Participants: 94 Evidence: moderate
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Using amyloid PET imaging as a single primary surrogate efficacy measure in Alzheimer's disease immunotherapy trials, as happened when the FDA granted accelerated approval of aducanumab, is unjustified. 1 key finding →
Evidence: low
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Here, we observed significant compromise in macroautophagy/autophagy in the brains of mlkl knockout (KO) mice, as evidenced by the downregulation of BECN1/Beclin1 and ULK1 (unc-51 like autophagy activating kinase 1). 5 key findings →
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.
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 →