In AD cases, pTau181 and ApoE4 levels were elevated, and the Aβ1-42/1-40 ratio was reduced. 5 key findings →
Participants: 27 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
In AD cases, pTau181 and ApoE4 levels were elevated, and the Aβ1-42/1-40 ratio was reduced. 5 key findings →
Participants: 27 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In Alzheimer's disease (AD), a single-nucleotide polymorphism in the gene encoding brain-derived neurotrophic factor (BDNF Val66Met ) is associated with worse impact of primary AD pathology (beta-amyloid, Aβ) on neurodegeneration and cognitive decline, rendering BDNF Val66Met an important modulating factor of cognitive impairment in AD. 5 key findings →
Participants: 149 Evidence: low
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Growing evidence indicates an association between cerebral microhemorrhages (MHs) and amyloid β accumulation in Alzheimer disease (AD), but to the knowledge of the authors the association with tau burden is unknown. 4 key findings →
Design: cohort study Evidence: moderate
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Clinical trials of anti-amyloid-β (Aβ) monoclonal antibodies in Alzheimer disease (AD) infer target engagement from Aβ positron emission tomography (PET) and/or fluid biomarkers such as cerebrospinal fluid (CSF) Aβ42/40. 2 key findings →
Evidence: moderate
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Symptomatic GRN carriers showed elevated WMHs, primarily in the frontal lobe, while no significant increase was observed in symptomatic C9orf72 or MAPT carriers. 5 key findings →
Participants: 763 Evidence: low
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Elevated microglial activation in the right amygdala-entorhinal-hippocampal complex of App NL-G-F mice is associated with better spatial learning. 5 key findings →
Design: cross-sectional Evidence: low
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Brain changes reminiscent of Alzheimer disease (AD) have been previously reported in a substantial portion of elderly cognitive healthy (HC) subjects. 4 key findings →
Evidence: low
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The present study explores the associations of soluble TREM2, an important regulator of microglial activity linked to Alzheimer's disease (AD), with other known inflammatory proteins in cerebrospinal fluid (CSF). 4 key findings →
Participants: 303 Evidence: low
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The patterns of FDG decline are distinct in these 2 genetically determined forms of AD. 1 key finding →
Design: cross-sectional Participants: 76 Evidence: low
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Recent work suggests that impairment in emotional processing, along with disinhibition, constitutes the necessary elements for CB in bvFTD. 4 key findings →
Participants: 87 Evidence: low
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Overall, 64% of PlwAD received at least one AD-Rx. 5 key findings →
Participants: 576 Evidence: low
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Alzheimer's disease (AD) and vascular dementia (VaD) together contribute to almost 90 % of all dementia cases leading to major health challenges of our time with a substantial global socioeconomic burden. 1 key finding →
Evidence: low
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Tauopathies, such as Alzheimer's disease and frontotemporal dementia, are common neurodegenerative diseases characterized by misfolding, hyperphosphorylation, and aggregation of tau. 5 key findings →
Evidence: low
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Global PSP prevalence ranges between 5-6.4 per 100,000, influenced by diagnostic criteria and healthcare infrastructure. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Lower cognitive levels in lonely and socially isolated patients suggest that these factors may contribute to dementia progression. 2 key findings →
Participants: 382 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
variants) was not associated with small vessel stroke (odds ratio [OR], 1.02 [95% CI, 0.95-1.10]), magnetic resonance imaging-confirmed lacunar stroke (OR, 0.95, [95% CI, 0.81-1.11]), nonlobar intracerebral hemorrhage (OR, 1.04 [95% CI, 0.72-1.50]), or vascular dementia (OR, 1.09 [95% CI, 0.95-1.25]). 5 key findings →
Evidence: low
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In vivo MRI biomarkers can support the diagnosis of early-onset cerebral amyloid angiopathy, which might already be present in pediatric Down syndrome patients. 2 key findings →
Participants: 12 Evidence: low
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Dementia is a growing challenge in Southeastern and Western Europe, with aging trends projected to accelerate in the former region. 5 key findings →
Evidence: low
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Several concepts, which in the aggregate get might be used to account for "resilience" against age- and disease-related changes, have been the subject of much research.
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Frailty in DS is associated with both ID severity and acquired cognitive decline. 5 key findings →
Design: cross-sectional Evidence: low
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Soluble triggering receptor expressed on myeloid cells 2 (sTREM2) levels in the cerebrospinal fluid (CSF) have been associated with Alzheimer disease (AD) status. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Die amyloide Selbstassemblierung von α‐Synuclein (αSyn) wird mit der Pathogenese der Parkinson‐Krankheit (PD) in Verbindung gebracht. 5 key findings →
Evidence: low
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Our findings support a broader interpretation of TBK1-associated neurodegeneration and highlight the importance of multimodal diagnostic approaches that integrate molecular, genetic, imaging, and neuropathological tools. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Die Frühphasen- & R1-Bilder korrelierten signifikant in allen Gruppen (Gesunde: r=0,68-0,84; AD: r=0,81-0,9; PSP-RS: r=0,81-0,86; FTD: r=0,76-0,82). 5 key findings →
Participants: 26 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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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.
1,034 records (3.7% 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 →