Alzheimer's disease (AD) is the most common cause of dementia. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
31,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
αB-crystallin (αB) is known as an intracellular Golgi membrane-associated small heat shock protein. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
PART and LATE patients exhibit Tau PET uptake similar to that of controls, except in the putamen. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Cerebrospinal fluid (CSF) total Tau levels vary widely in neurodegenerative disorders, thus being not useful in their discrimination over Alzheimer disease. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer disease (AD) is the leading cause of dementia globally and is defined by the presence of amyloid-β (Aβ) plaques and neurofibrillary tangles formed by the accumulation of phosphorylated tau (p-tau). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Parkinsons disease and dementia with Lewy bodies patients both demonstrated weaker global BOLD-CSF coupling compared to controls, with no detectable difference between patient groups. 4 key findings →
Participants: 39 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
PVeD reproducibly contextualized associations between plasma pTau217 and PET-defined Alzheimer pathology across cohorts with different participant composition, pTau217 assays, PET tracers, and cognitive measures. 2 key findings →
Participants: 602 Evidence: low
Full summary, score breakdown and related studies → Original source
A prespecified structure–reserve–glial profile captured reproducible cognitive variation beyond measured Alzheimer disease molecular pathology across two cohorts. 1 key finding →
Design: longitudinal study Participants: 436 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Complement-mediated neuroinflammation has been implicated in Alzheimer’s disease (AD), but its role during the pre-symptomatic phase of the disease remains unclear. 4 key findings →
Participants: 708 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Brain perfusion SPECT revealed AD-typical hypoperfusion patterns and demonstrated modest potential to estimate the presence or absence of Aβ deposition with left parietal rCBF. 5 key findings →
Participants: 88 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) pathology develops years in advance prior to its clinical presentation. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid regional extent and tau PET were associated with different features of dyadic CFI data: reporter balance and CFI burden across reporters, respectively. 4 key findings →
Design: cross-sectional Participants: 1,686 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease pathology and cognitive outcomes frequently diverge, yet current single-axis definitions cannot identify resilient (high pathology, preserved cognition) and resistant (high risk, low pathology) subgroups reliably at scale, obscuring the mechanisms that uncouple pathological burden from cognitive decline. 2 key findings →
Participants: 1,009 Evidence: moderate
Full summary, score breakdown and related studies → Original source
16/100
Alzheimer’s disease and cerebral amyloid angiopathy are characterized by the accumulation of amyloid-β (Aβ) species, yet the human fluid-physiological mechanisms that regulate soluble Aβ transport and clearance remain poorly understood. 3 key findings →
Participants: 502 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Structured Abstract INTRODUCTION Alzheimer’s disease (AD) progresses over decades, yet plasma biomarkers that resolve disease stage rather than simply detect disease remain scarce. 3 key findings →
Participants: 90 Evidence: moderate
Full summary, score breakdown and related studies → Original source
DPM is fundamentally constrained by dynamic range, variability, and test–retest reliability of the biomarker of interest. 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Semi-supervised multimodal fusion improves prediction and reveals interpretable imaging patterns that predict APOE4 and clinical diagnoses better than traditional approaches. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Precision medicine approaches require physiological effects to be informative when translated to the individual. 5 key findings →
Participants: 45 Evidence: low
Full summary, score breakdown and related studies → Original source
As the only central nervous system tissue that can be directly imaged non-invasively using widely available technology, the retina offers a uniquely accessible window into the brain. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We then integrated healthy retinal expression, AD retinal proteomics, and PD aqueous-humor proteomics with the brain-concordance results. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) pathology is increasingly recognized to manifest in the retina, offering a non-invasive window for early biomarker discovery. 2 key findings →
Design: longitudinal study Participants: 40 Evidence: moderate
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 31,380 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.
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 31,380 records, built mostly from automated pulls of Europe PMC (65.6% of the library) and OpenAlex (16.2%), 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.
1,048 records (3.3% of the library) are not peer-reviewed — 973 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