Rates of cognitive decline in Alzheimer's disease (AD) are extremely heterogeneous. 1 key finding →
Design: case-control study Participants: 3,397 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Rates of cognitive decline in Alzheimer's disease (AD) are extremely heterogeneous. 1 key finding →
Design: case-control study Participants: 3,397 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The literature has several methodological limitations including lack of sufficient algorithm development descriptions and standard definitions. 1 key finding →
Participants: 255 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
This study investigated a subtype of reactive astrocytes called A1 and discovered that they are induced by classically activated neuroinflammatory microglia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We sent invitations to 91,433 households; 5542 (6.1%) responded, 2120 completed the Baseline Survey (78.5% online; 21.5% via computer-assisted telephone interview), and 2087 were deemed eligible, yielding a response rate of 2.3%. 2 key findings →
Design: randomized controlled trial Participants: 374 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Synapse loss in Alzheimer's disease (AD) correlates with cognitive decline. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
A total of 14 participants (2 in part A and 12 in parts B and C) completed at least 12 months of follow-up and were included in the analyses. 5 key findings →
Participants: 14 Evidence: low
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Pathological hallmarks of Alzheimer's disease (AD) precede clinical symptoms by years, indicating a period of cognitive resilience before the onset of dementia. 4 key findings →
Evidence: low
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Alzheimer's disease (AD) is the most common cause of progressive intellectual failure in aged humans. 4 key findings →
Evidence: low
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The average CHADS2 score was 3.3 ± 1.3. After a diagnosis of dementia, 405 individuals (16%) persisted on warfarin therapy. 4 key findings →
Design: cohort study Participants: 2,572 Evidence: moderate
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Inclusion body myopathy associated with Paget disease of bone and frontotemporal dementia (IBMPFD) is a dominant progressive disorder that maps to chromosome 9p21.1-p12. 4 key findings →
Evidence: low
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Neuronal circuit assembly requires the fine balance between synapse formation and elimination. 4 key findings →
Evidence: low
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Disclosure (N = 194) and non-disclosure (N = 180) groups did not differ on IGT-AD (mean disclosure-non-disclosure difference [MD] at 6 weeks: -1.5, p = 0.14; 9 months: -1.2, p = 0.35; 15 months: -2.0, p = 0.07), IES-R (MD at 6 weeks: 0.00, p = 0.98; 9 months: 0.01, p = 0.84; 15 months: 0.03, p = 0.64), or change in secondary outcomes. 4 key findings →
Design: randomized controlled trial Participants: 194 Evidence: high
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As compared with placebo, semagacestat did not improve cognitive status, and patients receiving the higher dose had significant worsening of functional ability.
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Several members of the chemokine receptor family are used together with CD4 for HIV-1 entry into target cells. 4 key findings →
Evidence: low
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Neuronal hyperactivity is a key feature of early stages of Alzheimer's disease (AD). 4 key findings →
Evidence: low
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The number of patients surviving with congenital heart disease (CHD) has soared over the last 3 decades. 1 key finding →
Evidence: low
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Neurodegenerative diseases of the central nervous system progressively rob patients of their memory, motor function, and ability to perform daily tasks. 4 key findings →
Evidence: low
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Reprogramming somatic cells to induced pluripotent stem cells (iPSCs) resets their identity back to an embryonic age and, thus, presents a significant hurdle for modeling late-onset disorders. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In Alzheimer's disease (AD), pathological tau protein shows a progressive accumulation of post-translational modifications (PTMs), reflecting disease severity, progression, and prion-like activity. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Using human stem cell-derived neurons, we show that TDP-43 reduction induces cryptic splicing and downregulation of these genes, resulting in impaired excitability and synaptic transmission. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
TAR DNA binding protein-43 (TDP-43) is found in ubiquitinated inclusions (UBIs) in some frontotemporal dementias (FTD-U). 4 key findings →
Evidence: low
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The 4.2-kilodalton (kDa) polypeptide associated with the cerebral amyloid deposits of Alzheimer's disease (AD) derives from a much larger protein that is encoded by a gene on chromosome 21. 4 key findings →
Evidence: low
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Among most Latinos in northern Manhattan who learned they had an APOE ε4/ε4 genotype, disclosure did not provoke elevated levels of distress. 3 key findings →
Participants: 61 Evidence: low
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We found that pharmacological activation of TREM2 suppressed laser-induced choroidal neovessel formation. 4 key findings →
Evidence: low
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Deposition of amyloid filaments serves as a pathologic hallmark for some neurodegenerative disorders. 1 key finding →
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 →