31,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Tau is a hallmark pathology of Alzheimer's disease, and animal models have suggested that tau spreads from cell to cell through neuronal connections, facilitated by β-amyloid (Aβ). 3 key findings →
Participants: 312 Evidence: low
Full summary, score breakdown and related studies → Original source
Dichotomising these biomarkers as normal or abnormal results in eight possible profiles. 2 key findings →
Participants: 435 Evidence: low
Full summary, score breakdown and related studies → Original source
A growing body of evidence suggests that the dysregulation of neuronal iron may play a critical role in Alzheimer's disease. 3 key findings →
Participants: 236 Evidence: low
Full summary, score breakdown and related studies → Original source
In Alzheimer's disease (AD), deposition of insoluble amyloid-β (Aβ) is followed by intracellular aggregation of tau in the neocortex and subsequent neuronal cell loss, synaptic loss, brain atrophy, and cognitive impairment. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
CNS inflammation is a key factor in Alzheimer's Disease (AD), but its relation to pathological Aβ, tau, and APOE4 is poorly understood, particularly prior to the onset of cognitive symptoms. 3 key findings →
Design: cross-sectional Participants: 57 Evidence: low
Full summary, score breakdown and related studies → Original source
Centiloid values < 10 accurately reflected the absence of any neuritic plaque and > 20 CL indicated the presence of at least moderate plaque density, but approximately 50 CL or more best confirmed both neuropathological and clinicopathological diagnosis of Alzheimer's disease. 5 key findings →
Participants: 49 Evidence: low
Full summary, score breakdown and related studies → Original source
Vascular brain injury and Aβ were independent in both cognitively normal and impaired participants. 5 key findings →
Design: cross-sectional Participants: 30 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer disease (AD) and related tauopathies are histopathologically characterized by a specific type of slow and progressive neurodegeneration, which involves the abnormal hyperphosphorylation of the microtubule associated protein (MAP) tau. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Increased (11)C-DED binding throughout the brain of the MCI (11)C-PIB+ patients potentially suggests that astrocytosis is an early phenomenon in AD development. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The amyloid cascade hypothesis is widely accepted as the centerpiece of Alzheimer disease (AD) pathogenesis. 3 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
SUVs in the pons and the inferior cerebellum indicated consistent clearance across all 51 subjects. 5 key findings →
Participants: 19 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This human study is based on an established cohort of "SuperAgers," 80+-year-old individuals with episodic memory function at a level equal to, or better than, individuals 20-30 years younger. 4 key findings →
Participants: 21 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Increased Aβ burden was observed in TBI. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Disease-specific patterns of functional network topology and connectivity alterations were observed in patients with EOAD and bvFTD. 3 key findings →
Participants: 37 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In this patient, the clinical disease symptoms progressed rapidly in life, paralleled with an annual increase of tau PET retention of 20% to 40% in many cortical regions. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In both cohorts, CSF MTBR-tau243 was associated with tau-PET temporal meta-ROI burden (BioFINDER-2: β = 1.1, p = < 0.0001 and Knight-ADRC: β = 0.7, p = < 0.0001), and this association did not differ by sex (BioFINDER-2 β = 0.04, p = 0.6 and Knight-ADRC: β = 0.009, p = 0.9). 3 key findings →
Design: cross-sectional Participants: 446 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
More specifically, 18F-AV-1451 binding was significantly increased in patients with Alzheimer's disease, relative to patients with progressive supranuclear palsy and with control subjects, in the hippocampus and in occipital, parietal, temporal, and frontal cortices (t's > 2.2, P's < 0.04). 4 key findings →
Participants: 15 Evidence: low
Full summary, score breakdown and related studies → Original source
Tau vulnerability in women is not just limited to the medial temporal lobe and significantly contributed to greater risk of faster cognitive decline. 2 key findings →
Participants: 55 Evidence: moderate
Full summary, score breakdown and related studies → Original source
We found significant group-wise differences in 11C-PK-11195 binding between each patient group and controls in frontotemporal regions, in both a regions-of-interest analysis and in the comparison of principal spatial components of binding. 18F-AV-1451 binding was increased in semantic variant primary progressive aphasia compared to controls in the temporal regions, and both semantic variant primary progressive aphasia and behavioural variant frontotemporal dementia differed from controls in the expression of principal spatial components of binding, across temporal and frontotemporal cortex, respectively. 2 key findings →
Participants: 31 Evidence: low
Full summary, score breakdown and related studies → Original source
We provide the first evidence for the capability of a high-resolution positron emission tomographic (PET) imaging system in quantitatively mapping amyloid accumulation in living amyloid precursor protein transgenic (Tg) mice. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Subjects without amyloid, including three with pathologically confirmed corticobasal degeneration, showed greater regional 18F-AV-1451 retention and associated regional atrophy in areas commonly associated with corticobasal degeneration pathology than healthy control subjects [retention was higher compared to healthy controls (P = 0.0011), driven especially by the precentral gyrus (P = 0.011) and pallidum (P < 0.0001), and greater atrophy was seen in subjects compared to control subjects (P = 0.0004)]. 3 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
See Vandenberghe and Schaeverbeke (doi:10.1093/awx065) for a scientific commentary on this article. 3 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
In the preclinical phase of both sporadic and autosomal dominant AD, multiple behavioral features were associated with AD pathology. 4 key findings →
Participants: 117 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The relationship between magnetic resonance imaging (MRI)-visible enlarged perivascular spaces (EPVS) and Aβ and tau deposition is poorly investigated in cognitively normal older population. 4 key findings →
Participants: 43 Evidence: low
Full summary, score breakdown and related studies → Original source
Although overlap occurs between groups, PD patients with probable RBD may have greater density and range of synuclein pathology on autopsy. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
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 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.
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