27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Amyloid plaques are a neuropathologic hallmark of Alzheimer's disease (AD), which can be imaged through positron emission tomography (PET) technology using radiopharmaceuticals that selectively bind to the fibrillar aggregates of amyloid-β plaques (Amy-PET). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Using the calibration images, there was a very strong agreement, and very little bias between the centiloid values computed using CapAIBL and those computed using the standard method with R2 > 0.97 across all tracers. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Fixed tissue sections of frontal cortex and caudate from 10 of the AD cases were processed for microscopy using fluorescent derivatives of flutemetamol (cyano-flutemetamol) and PiB (cyano-PiB) and compared to Aβ immunohistochemistry and pan-amyloid (X-34) histology. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tau aggregates accumulate in the Alzheimer's disease (AD) brain according to the established Braak staging scheme and spread from transentorhinal over limbic regions to the neocortex. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
[ 18 F]-AV-1451 is a leading tracer used with positron emission tomography (PET) to quantify tau pathology. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our results are consistent with the supposition that both Aβ and tau are necessary for memory decline in the preclinical stages of AD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Currently, over five million Americans suffer with Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The relationships between β-amyloid (Aβ), tau and neurodegeneration within Alzheimer's Disease pathogenesis are not fully understood. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our study identified a synergistic effect of amyloid and tau deposits and demonstrated, for the first time, in normal elderly its link to AD-like hypometabolism and to AD-like memory decline. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
(18)F-flutemetamol uptake can be readily quantified. 3 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
With the advent of PET imaging in 1976, 2-deoxy-2-[18F]fluoro-D-glucose (FDG)-PET became the preferred method for in vivo investigation of cerebral processes, including regional hypometabolism in Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
All four plasma markers significantly correlated with 18F-florbetapir SUVR (|β| = 0.40-0.49; p < .05). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
High diagnostic sensitivity and negative predictive value (NPV) for Aβ-PET positivity were observed, consistent with the clinical performance of other plasma LC-MS/MS assays, but with greater separation between Aβ42/40 values for individuals with positive vs negative Aβ-PET results. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid β 42/40 concentration quotient has been empirically shown to improve accuracy of the neurochemical diagnostics of Alzheimer's Disease (AD) compared to the Aβ42 concentration alone, but this improvement in diagnostic performance has not been backed up by a theoretical argumentation so far. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A systematic interpretation strategy could support accurate diagnosis and staging of AD. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Do MRI-based metrics of a CSF-dynamics disorder, disproportionately enlarged subarachnoid-space hydrocephalus (DESH), correlate with discordant amyloid biomarkers (low CSF β-amyloid 1-42, normal Aβ-PET scan)? 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
For many years Alzheimer's disease (AD) was associated with the dementia stage of the disease, the tail end of a pathophysiological process that lasts approximately two decades. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Transgenic animals displayed higher total exposure, calculated as the AUC based on SUV determined at 24h, 48h, and 72h post injection, of PET radioligand [124I]mAb1729-scFv8D3CL than WT mice. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tau protein plays a vital role in maintaining the structural and functional integrity of the nervous system; however, hyperphosphorylation or abnormal phosphorylation of tau protein plays an essential role in the pathogenesis of several neurodegenerative disorders. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
SUVRs in target regions were relatively stable 60 to 90 min post-injection, with the exception of very high binders who continued to show increases over time. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Twenty-four percent (11 of 45) were β-amyloid-positive. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The enhanced ultra-low-dose τ images showed apparent noise reduction compared with the ultra-low-dose images. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
High tau PET signal was generally observed in the lateral temporal and parietal cortices, with uptake in the occipital cortex in one subject. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Baseline tau-PET was strongly associated with the subsequent cognitive decline in regions that are usually associated with each cognitive domain. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This international consensus and practice guideline will help to promote the standardized use of 18F-flortaucipir PET in patients with AD. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
10 of the 319 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 →