28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Alzheimer’s disease (AD) is pathologically characterized by the accumulation of amyloid-β (Aβ) plaques, neurofibrillary tangles and widespread neuronal loss in the brain. 5 key findings →
Design: longitudinal study Participants: 12 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Elevated levels of AD biomarker p-tau181/Aβ42, by itself or combined with a low Aβ42/Aβ40 level, predicts clinically diagnosed AD. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Over 20% of patients with Alzheimer's disease (AD) worldwide are Chinese, although the efficacy of existing blood-based measures of AD biomarkers is largely unknown in Asian cohorts. 3 key findings →
Design: cross-sectional Participants: 425 Evidence: moderate
Full summary, score breakdown and related studies → Original source
To evaluate the clinical importance of cerebrospinal fluid (CSF) phosphorylated tau 181 (p-tau181) in mild cognitive impairment (MCI), Alzheimer's disease (AD) and other dementias, more specifically: frontotemporal degeneration (FTD), dementia with Lewy bodies (DLB), vascular dementia (VaD) and Parkinson's disease (PD) with dementia (PDD). 2 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Relative to controls, greater Alzheimer's disease pathology (lower amyloid-β 42 /amyloid-β 40 , higher phosphorylated-tau-181) and synaptic degeneration (neurogranin) biomarker concentrations were associated with more adverse white matter metrics (e.g. lower neurite density, higher mean diffusivity) in patients with asthma. 4 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma p-tau217 and p-tau181 effectively predict Aβ+ among culturally different Asian populations. 1 key finding →
Participants: 270 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma p-tau217 measured using the Lumipulse platform shows promise as an accurate biomarker of preclinical AD pathology. 4 key findings →
Design: prospective cohort Evidence: moderate
Full summary, score breakdown and related studies → Original source
Recently, conceptual systems for the in vivo staging of Alzheimer's disease (AD) using fluid biomarkers have been suggested. 4 key findings →
Participants: 219 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Among the 128 study participants, the 104 patients with early PD had a different CSF pattern compared with the 13 patients with progressive supranuclear palsy (baseline area under the receiver operating characteristic curve, 0.87; P < .0001) and the 30 control participants (baseline area under the receiver operating characteristic curve, 0.69; P = .0021). 2 key findings →
Design: cohort study Participants: 104 Evidence: moderate
Full summary, score breakdown and related studies → Original source
There is evidence that serum NfL is increased more than a decade before the onset of clinical symptoms in FAD and rises thereafter. 3 key findings →
Design: longitudinal study Participants: 61 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Our results support the link between OCR and CR. 5 key findings →
Design: cross-sectional Participants: 2,369 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Type 2 diabetes is associated with altered plasma concentrations of Aβ peptides and is an important source of variation that needs to be taken into account when considering plasma Aβ peptides as biomarkers for Alzheimer's disease. 4 key findings →
Participants: 194 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Perioperative changes in plasma amyloid do not appear to be associated with postoperative delirium. 5 key findings →
Design: cohort study Participants: 100 Evidence: moderate
Full summary, score breakdown and related studies → Original source
In AD-converters (N = 158, 377 samples), higher plasma GFAP levels are observed 10 years prior to the onset of cognitive impairment due to AD compared with individuals who remain cognitively unimpaired (N = 160, 379 samples). 3 key findings →
Design: case-control study Participants: 158 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Although liver dysfunction has been implicated in Alzheimer's disease (AD), it remains unknown how liver disease may influence the trajectory of brain and cognitive changes in older adults. 3 key findings →
Design: longitudinal study Participants: 780 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The TBSS contrasts with by ANOVA F -test has identified strongly significant clusters in the forceps minor, inferior longitudinal fasciculus, inferior fronto-occipital fasciculus, and cingulum gyrus. 5 key findings →
Design: longitudinal study Participants: 19 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Studies evaluating the diagnostic test accuracy of plasma phosphorylated tau (p-tau) and amyloid beta (Aβ) tests (p-tau217, %p-tau217, p-tau181, p-tau231, and Aβ42/Aβ40) compared to reference standard tests (cerebrospinal fluid [CSF] AD biomarkers, amyloid positron emission tomography [PET], or neuropathology) in individuals with cognitive impairment (mild cognitive impairment or dementia) in specialized care settings were included. 4 key findings →
Design: meta-analysis Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Cerebrospinal fluid (CSF) α-synuclein (α-syn) seed amplification assays (SAAs) can detect Lewy body pathology (LBP) with high accuracy but are invasive and costly. 2 key findings →
Design: cohort Participants: 1,567 Evidence: early
Full summary, score breakdown and related studies → Original source Free full text
Self-report of poor sleep was associated with greater AD-related pathology in cognitively healthy adults at risk for AD. 3 key findings →
Participants: 101 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
We enrolled a cohort of 1070 PSEN1 E280A mutation carriers and 1074 non-carriers with baseline assessments; of these participants, longitudinal measures (with a mean follow-up of 6 years) were available for 242 mutation carriers and 262 non-carriers. 1 key finding →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Both CSF p-tau and NfL correlate with disease severity and rate of disease progression in PSP. 4 key findings →
Participants: 50 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Pericyte damage, reflected by CSF PDGFRβ, may be involved in age-related BBB disruption together with neuroinflammation, but is not related to Alzheimer-related pathologic changes. 2 key findings →
Participants: 408 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Disease-modifying therapies for Alzheimer's disease (AD) are likely to be most beneficial when initiated in the presymptomatic phase. 2 key findings →
Design: cross-sectional Participants: 567 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Plasma p-tau217 levels showed a significant increase across advancing AD stages, with all between-group comparisons remaining significant after false discovery rate adjustment ( p p = 0.002) and CSF p-tau181 (β = 3.2, 95% CI 1.4-5.0, p = 0.001). 5 key findings →
Design: cohort study Participants: 731 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
We constructed models for MCI and mild dementia that predict MMSE over time. 1 key finding →
Design: longitudinal study Participants: 961 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
10 of the 3,322 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
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 →