Baseline sleep disturbance was associated with a faster rate of longitudinal CSF Aβ42 decline. 4 key findings →
Design: longitudinal study Participants: 1,205 Evidence: moderate
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.
Independent of t-tau and TCBV, epigenetic age measures were associated with time to MCI, AD, and all-cause dementia and baseline cognition, but not with cognitive trajectories. 5 key findings →
Design: longitudinal study Participants: 2,606 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Midlife p-tau181 was associated with faster 11-year memory decline beginning 20 years later in the ARIC cohort, which underscores a potentially long prodromal phase of cognitive decline that could precede dementia onset. 5 key findings →
Design: prospective cohort Participants: 920 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Three AD subtypes were identified. Subtype 1, enriched in RNA metabolism pathways, showed the mildest atrophy and slowest cognitive decline. 5 key findings →
Design: longitudinal study Participants: 550 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The causes of late onset Alzheimer disease (LOAD) are not known but several recent lines of evidence implicate the adaptive immune system. 3 key findings →
Design: longitudinal study Participants: 72 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The NPTX2/p-tau ratio enhanced diagnostic performance of standalone NPTX2 and p-tau, particularly for DLB and FTLDrs (area under the curve [AUC]NPTX2/p-tau = 0.78-0.79 vs. AUCNPTX2 = 0.63-0.70 and AUCp-tau = 0.59-0.75), and was more strongly associated with cognition. 4 key findings →
Participants: 688 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Prion diseases can mimic Alzheimer disease (AD) at presentation. 4 key findings →
Design: cohort study Participants: 345 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
False-positive (FP) plasma results may lead to overtreatment and false-negative (FN) results to missed or delayed disease-modifying therapies. 5 key findings →
Participants: 706 Evidence: low
Full summary, score breakdown and related studies → Original source
With blood-based phosphorylated tau biomarkers soon to be used for diagnosis of Alzheimer disease, analyzing tau levels in other conditions could enhance biomarker interpretability. 4 key findings →
Participants: 27 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
53/100
Moreover, there is limited knowledge regarding associations with domain-specific cognitive decline and modifying effects of key individual characteristics. 4 key findings →
Design: cohort study Participants: 2,008 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Late-onset unexplained epilepsy (LOUE) represents a substantial proportion of epilepsies with onset after 50 years and often manifests as temporal lobe epilepsy (LO-TLE). 4 key findings →
Design: cohort study Participants: 18 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
52/100
Prion disease and Alzheimer disease (AD) are common causes of rapidly progressive dementia (RPD). 4 key findings →
Design: systematic review Participants: 15 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Sleep spindles (SPs) and slow oscillations (SOs) are linked to cognition and neurodegeneration; however, their relationship with CSF orexin concentrations in symptomatic AD has not been characterized. 4 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In vivo biomarkers for detecting neuropathologies from repetitive head impacts (RHI), including chronic traumatic encephalopathy (CTE), are needed. 4 key findings →
Design: case-control study Participants: 231 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
This study investigated whether longitudinal changes in CSF AD biomarkers were associated with 18 F-MK6240 tau PET measures in early Braak stage subregions. 4 key findings →
Design: cross-sectional Participants: 78 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Elevated blood levels of phosphorylated tau (p-tau) are diagnostic of Alzheimer disease and are associated with the deposition of amyloid-β in the cerebral neuropil. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer disease (AD) is the most common cause of dementia in the world and its prevalence is increasing and it has important public health consequences. 4 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Cerebral amyloid angiopathy (CAA) is currently diagnosed using MRI-based Boston criteria. 4 key findings →
Design: cohort study Participants: 102 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The study aim is to investigate whether blood biomarkers (BBMs) of Alzheimer's disease (AD) pathology are associated with postoperative cognitive dysfunction (POCD) after cardiac surgery. 4 key findings →
Participants: 394 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Postoperative Cognitive Dysfunction (POCD) is a common complication in older adults undergoing major surgery and is associated with prolonged recovery and long-term cognitive decline. 4 key findings →
Design: systematic review Participants: 705 Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Impaired lung function (ILF) has been associated with cognitive decline and dementia risk in multiple cohorts, yet the role of circulating Alzheimer disease (AD) biomarkers in this relationship is not well understood. 4 key findings →
Participants: 4,072 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Individuals with autosomal dominant Alzheimer's disease (ADAD) arising from mutations in PSEN1, PSEN2, or APP exhibit variability in clinical presentation. 4 key findings →
Participants: 2,338 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
BackgroundAmyloid-negative tau-related neurodegeneration represents a non-Alzheimer biomarker-defined profile; however, its clinical heterogeneity and prognostic relevance remain unclear within Alzheimer's disease-related frameworks. 4 key findings →
Design: cohort study Participants: 1,280 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
No amyloid-related imaging abnormalities occurred. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Plasma biomarkers such as phospho-tau species are increasingly used in clinical practice for the diagnosis of Alzheimer disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
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
- Randomized / 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
- Multicenter 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