27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
BACKGROUNDPeople with type 2 diabetes mellitus (T2DM) are at higher risk of cerebral small vessel disease and left ventricular hypertrophy (LVH), potentially contributing to cognitive decline and dementia. 5 key findings →
Design: cohort study Participants: 62 Evidence: moderate
Full summary, score breakdown and related studies → Original source
O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=113 SRC="FIGDIR/small/26361997v1_ufig1.gif" ALT="Figure 1"> View larger version (32K): org.highwire.dtl.DTLVardef@1dac0d9org.highwire.dtl.DTLVardef@aaf8f2org.highwire.dtl.DTLVardef@be10a1org.highwire.dtl.DTLVardef@35c7be_HPS_FORMAT_FIGEXP M_FIG C_FIG BACKGROUNDThe effect of neurovascular health on cardiovascular outcomes is not well-known. 4 key findings →
Participants: 3,263 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
ResultsThe CNR2 missense variant rs4649124 was associated with increased vascular dementia risk (BH-adjusted P = 0.049) after correction at the 5% false discovery rate (FDR) threshold, with additional associations at the 10% FDR threshold for all-cause dementia risk (BH-adjusted P = 0.051) and lower circulating APP (BH-adjusted P = 0.088) and BDNF (BH-adjusted P = 0.083) levels. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
BackgroundAnti-amyloid-{beta} (A{beta}) monoclonal antibodies are disease-modifying treatments for early Alzheimers disease but are associated with amyloid-related imaging abnormalities (ARIA) and intracranial hemorrhage (ICH). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
INTRODUCTIONIndividuals with Alzheimers disease (AD) exhibit substantial heterogeneity in the severity of vascular changes and neurodegeneration, making the identification of biologically meaningful subtypes across the AD spectrum critical for improving prognosis and tailoring interventions. 1 key finding →
Design: longitudinal study Participants: 1,396 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
BackgroundClonal haematopoiesis (CH), the age-related expansion of mutated blood stem cells, is detectable in around 10% of people in their seventies, rises steeply with age, and is associated with several diseases. 5 key findings →
Design: longitudinal study Participants: 1,091 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
INTRODUCTIONDetermining whether plasma biomarkers are preferentially associated with Alzheimers disease (AD)-related rather than age-related brain atrophy patterns may clarify their prognostic and diagnostic clinical use. 5 key findings →
Design: cross-sectional Participants: 818 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Neuroinflammation is a principal driver of brain atrophy and cognitive decline in Alzheimers disease (AD). 2 key findings →
Participants: 49 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
MTD showed excellent discrimination of CU versus MCI/DEM (AUC=.89; 95% CI=.87-.92), and discriminability remained high for CU versus MCI (AUC=.88; 95% CI=.85-.92). 5 key findings →
Design: cohort study Participants: 1,224 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Biological aging is the correlated decline of multi-organ system integrity central to the etiology of many age-related diseases. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
While hippocampal (H) and inferior parietal lobule (IPL) atrophy are used routinely in Alzheimer's disease (AD) diagnostics, the role of enlarged choroid plexus (ChP) remains unclear. 2 key findings →
Participants: 872 Evidence: moderate
Full summary, score breakdown and related studies → Original source
This study explored the role of the ubiquitin-proteasome system (UPS) in dominantly inherited Alzheimer's disease (DIAD) by examining changes in cerebrospinal fluid (CSF) levels of UPS proteins along with disease progression, AD imaging biomarkers (PiB PET, tau PET), neurodegeneration imaging measures (MRI, FDG PET), and Clinical Dementia Rating® (CDR®). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
These findings support a model in which p-tau217 specifically tracks amyloid-driven pathological progression, while markers of neurodegeneration reflect broader age-related processes that are not associated with APOE genotype. 3 key findings →
Design: longitudinal study Participants: 60 Evidence: moderate
Full summary, score breakdown and related studies → Original source
TSE showed stronger unadjusted associations than SUVR in selected region- and outcome-specific comparisons, supporting its potential as a complementary measure. 2 key findings →
Participants: 682 Evidence: low
Full summary, score breakdown and related studies → Original source
ADNI identified task-dependent performance boundaries, particularly attenuated conditional T discrimination within A+. 2 key findings →
Design: post-hoc analysis Participants: 1,097 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Basal ganglia iron serves as a stage-dependent mediator linking pTau217 to hippocampal neurodegeneration, with prodromal AD potentially indicating a particularly vulnerable stage for iron-targeted interventions and iron profiling for patient stratification. 1 key finding →
Participants: 94 Evidence: low
Full summary, score breakdown and related studies → Original source
Tau-PET subtype modified the p-tau217–memory association, suggesting that the cognitive implications of plasma p-tau217 may vary with tau topography. 4 key findings →
Design: cross-sectional Participants: 396 Evidence: moderate
Full summary, score breakdown and related studies → Original source
WM fALFF was significantly associated with GFAP (partial RZ = 5.35%), amyloid PET (partial RZ = 2.17%), tau PET (partial RZ = 3.52%), executive function (partial RZ = 2.61%), and mPACC (partial RZ = 3.53%). 4 key findings →
Participants: 108 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease is diagnosed after a decade-long phase in which pathology accumulates; current markers show that pathology is present, but not how far it has advanced. 5 key findings →
Participants: 609 Evidence: low
Full summary, score breakdown and related studies → Original source
Physiological pulsations maintaining brain neurofluidic homeostasis are altered early in the course of Alzheimer’s disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
These findings support MRI-derived LC intensity as a marker of early AD-related processes and suggest that LC intensity may provide complementary information not captured by plasma pTau 217 alone. 4 key findings →
Design: longitudinal study Participants: 163 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Limbic-predominant age-related TDP-43 encephalopathy neuropathologic change (LATE-NC) frequently co-occurs with Alzheimer’s disease (AD) pathology and has been studied mainly in older populations. 3 key findings →
Participants: 196 Evidence: low
Full summary, score breakdown and related studies → Original source
[ 18 F]Tauvid and [ 18 F]MK6240 capture largely overlapping patterns of tau pathology, but differ notably in the magnitude of off-target binding. 3 key findings →
Participants: 681 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Tau PET burden is associated with subsequent cognitive decline in Alzheimer's disease, motivating forecasts for monitoring and studies of spatially targeted therapies. 3 key findings →
Participants: 168 Evidence: low
Full summary, score breakdown and related studies → Original source
Brain positron emission tomography (PET) imaging is a valuable tool which allows visualization of the pathological structures inside the living patients’ brains. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
10 of the 2,885 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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 →