The C9orf72 expansion is a common cause of ALS and FTLD, but not of AD or PD. 4 key findings →
Participants: 520 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
30,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
The C9orf72 expansion is a common cause of ALS and FTLD, but not of AD or PD. 4 key findings →
Participants: 520 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The tau gene has been found to be the locus of dementia with rigidity linked to chromosome 17. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Common single nucleotide polymorphisms in the SORL1 gene have been associated with late onset Alzheimer disease (LOAD), but causal variants have not been fully characterized nor has the mechanism been established. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
TREM2 is a pattern recognition receptor, expressed on microglia and myeloid cells, detecting lipids and Aβ and inducing an innate immune response. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The mechanisms by which trisomy 21 leads to the characteristic Down syndrome (DS) phenotype are unclear. 5 key findings →
Participants: 685 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The ε4 allele of the apolipoprotein E gene (APOE ε4) is associated with an additional risk for AD. 5 key findings →
Design: cross-sectional Participants: 240 Evidence: low
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We have characterised the proteolytic cleavage events responsible for the shedding of triggering receptor expressed on myeloid cells 2 (TREM2) from primary cultures of human macrophages, murine microglia and TREM2-expressing human embryonic kidney (HEK293) cells. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In the initial kindred of ten affected Italian individuals (mean age of disease onset 59·8 years [SD 8·7]), we detected significant linkage of Parkinson's disease to chromosome 14 and nominated LRP10 as the disease-causing gene. 2 key findings →
Evidence: low
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Abundant tau-positive neurofibrillary lesions constitute a defining neuropathological characteristic of Alzheimer's disease. 4 key findings →
Evidence: low
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NfL holds potential as a blood-based biomarker for symptomatic genetic FTD carriers, with moderate accuracy to distinguish PPD from mild forms including C9orf72 . 3 key findings →
Participants: 474 Evidence: low
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Microglia are active modulators of Alzheimer's disease but their role in relation to amyloid plaques and synaptic changes due to rising amyloid beta is unclear. 4 key findings →
Evidence: low
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Mutation in the triggering receptor expressed on myeloid cells (TREM) 2 gene has been identified as a risk factor for several neurodegenerative diseases including Alzheimer's disease (AD). 4 key findings →
Participants: 299 Evidence: low
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Astrocytes contribute to a variety of functions in the brain, including homeostasis, synapse formation, plasticity, and metabolism. 3 key findings →
Evidence: moderate
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The ATP-binding cassette transporter A7 (ABCA7) has been identified as a susceptibility factor of late onset Alzheimer disease in genome-wide association studies. 2 key findings →
Evidence: low
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The proteolytic processing of amyloid precursor protein (APP) to generate the neurotoxic amyloid β (Aβ) peptide is central to the pathogenesis of Alzheimer disease (AD). 4 key findings →
Evidence: low
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We hypothesized that de novo variants (DNV) might participate in the genetic determinism of sporadic early-onset Alzheimer disease (EOAD, onset before 65 years). 4 key findings →
Evidence: low
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The derivation of microglia from human stem cells provides systems for understanding microglial biology and enables functional studies of disease-causing mutations. 4 key findings →
Evidence: low
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Multiple lines of evidence suggest that specific subtypes of age-related cataract (ARC) and Alzheimer disease (AD) are related etiologically. 5 key findings →
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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We have characterized a cluster of single immunoglobulin variable (IgV) domain receptors centromeric of the major histocompatibility complex (MHC) on human chromosome 6. 4 key findings →
Evidence: low
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Genetic variation in the APOE gene and variation in chromosome 21 genotypes, including the APP locus, may influence age-associated cognitive decline in adults with Down syndrome. 3 key findings →
Design: longitudinal study Evidence: moderate
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Neuroinflammation and activation of innate immunity are early events in neurodegenerative diseases including Alzheimer's disease (AD). 4 key findings →
Evidence: low
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Early isolated functional disruptions in salience/visual networks were present in asymptomatic carriers, along with anterior cingulate gray matter reductions. 5 key findings →
Evidence: low
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Recent studies have shown that neurofibrillary tangles are frequently accompanied by alpha-synuclein inclusions in sporadic and familial Alzheimer disease, in Down syndrome, in progressive supranuclear palsy, and Parkinsonism dementia complex of Guam. 2 key findings →
Evidence: low
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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
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 30,980 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 30,980 records, built mostly from automated pulls of Europe PMC (65.2% of the library) and OpenAlex (16.4%), 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.
1,040 records (3.4% of the library) are not peer-reviewed — 965 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events