Presenilin1 (PSEN1) gene is the most common known genetic cause of early-onset familial Alzheimer's disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Presenilin 2 gene (PSEN2) mutations account for <5% of all early-onset familial Alzheimer's disease (EOFAD) cases and only 13 have strong evidence for pathogenicity. 1 key finding →
Participants: 19 Evidence: low
Full summary, score breakdown and related studies → Original source
We report a case of EOAD having a pathogenic PSEN1 (Trp165Cys) confirmed with in silico and in vitro predictions. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
A pathogenic mutation in the PSEN2 gene in a Korean patient associated with EOAD was identified. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Familial Alzheimer's disease (FAD) is caused by autosomal dominant mutations in the PSEN1, PSEN2 or APP genes, giving rise to considerable clinical and pathological heterogeneity in FAD. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
We identified two novel heterozygous mutations in two unrelated patients, Cys139Arg in the PGRN gene and Val412Ile in the PSEN1 gene. 4 key findings →
Participants: 17 Evidence: low
Full summary, score breakdown and related studies → Original source
Due to commonalities in pathophysiology, age-related macular degeneration (AMD) represents a uniquely accessible model to investigate therapies for neurodegenerative diseases, leading us to examine whether pathways of disease progression are shared across neurodegenerative conditions. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A repeat expansion in the C9orf72 (C9) gene is the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Retromer controls cellular homeostasis through regulating integral membrane protein sorting and transport and by controlling maturation of the endo-lysosomal network. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Lysosomal dysfunction in myeloid cells is increasingly implicated in neurodegenerative diseases. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tau is one of several proteins associated with frontotemporal dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
To assess the ability of [18F]PI-2620 to detect regional tau burden in non-Alzheimer's disease tauopathies compared with Alzheimer's disease, patients with progressive supranuclear palsy (n = 3), corticobasal syndrome (n = 2), corticobasal degeneration (n = 1) or Alzheimer's disease (n = 8), and healthy controls (n = 7) were recruited. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Radiotracer [18F]Flortaucipir is an FDA-approved diagnostic agent for PET imaging of density and distribution of abnormal tau protein deposition (tauopathies) in Alzheimer's disease. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
[18F]Flortaucipir is a PET tau tracer used to visualize tau binding in Alzheimer's disease (AD) in vivo. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
APOE ε4 showed significant (P < .05) associations with tau deposition across all disease stages. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Most participants were cognitively normal (427 of 491 [87%]) and the mean age was 69.0 ± 8.8 years. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
45/100
SUVr calculated by our method and CortexID were highly correlated (R2 = 0.9657). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease-related atrophy in the posterior cingulate cortex, a key node of the default mode network, is present in the early stages of disease progression across clinical phenotypic variants of the disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
DTI revealed significant differences in white matter diffusivity between CCD and cognitively healthy aged dogs. 5 key findings →
Participants: 20 Evidence: low
Full summary, score breakdown and related studies → Original source
We found that patients with T2DM exhibited cognitive function declines and functional connectivity disruptions within the default mode network, left frontal parietal network, and sensorimotor network. 3 key findings →
Participants: 37 Evidence: low
Full summary, score breakdown and related studies → Original source
There was a significant association between greater Affective factor symptoms and reduced FPCN connectivity (p = 0.03). 5 key findings →
Participants: 42 Evidence: low
Full summary, score breakdown and related studies → Original source
Regional functional connectivity (FC) of 39 patients with Alzheimer's disease (AD), 23 patients with mild cognitive impairment (MCI), and 43 healthy elderly controls was studied using resting-state functional magnetic resonance imaging (rs-fMRI). 4 key findings →
Participants: 39 Evidence: low
Full summary, score breakdown and related studies → Original source
Preserving brain health is essential to maintaining quality of life and cognitive function with age. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
45/100
It remains unclear why β-amyloid (Aβ) plaque, a hallmark pathology of Alzheimer's disease (AD), first accumulates cortically in the default mode network (DMN), years before AD diagnosis. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Over the past decade, ocular imaging strategies have greatly advanced the diagnosis and follow-up of patients with optic neuropathies. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Where “Free full text” comes from
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
How the 0–100 score works — and why some entries are capped
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.
- Journal tier up to 10 pts
- Journal's citation record up to 4 pts
- Study design up to 12 pts
- Strength of evidence up to 5 pts
- Peer-review validation up to 10 pts
- How recent up to 5 pts
- Sample size up to 4 pts
- Effect reported up to 3 pts
- Studied in people up to 3 pts
- Randomised / blinded up to 2 pts
- Times cited up to 7 pts
- Citations per year up to 5 pts
- Impact for its field and year up to 6 pts
- Cited by studies here up to 6 pts
- Still being cited up to 4 pts
- Senior author's track record up to 4 pts
- Institution's track record up to 3 pts
- Multi-centre collaboration up to 3 pts
- Indexed in PubMed up to 2 pts
- Free to read up to 2 pts
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 28,580 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.
What this library is — and isn't
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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 (3.6% 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 →