27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
A multi-stage variable selection method is introduced for detecting association signals in structured brain-wide and genome-wide association studies (brain-GWAS). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We studied small vessel disease (SVD) pathology in Familial Alzheimer's disease (FAD) subjects carrying the presenilin 1 (PSEN1) p.Glu280Ala mutation in comparison to those with sporadic Alzheimer's disease (SAD) as a positive control for Alzheimer's pathology and Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL) bearing different NOTCH3 mutations, as positive controls for SVD pathology. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Presenilin 1 (PSEN1) mutations are a major cause of familial Alzheimer's disease. 2 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
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
This article reviews tau PET imaging with an emphasis on first-generation and second-generation tau radiotracers and their application in neurodegenerative disorders, including Alzheimer's disease and non-Alzheimer's disease tauopathies. 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
Positron emission tomography (PET) imaging allows monitoring the progression of amyloid aggregation in the living brain. [18F]-Flortaucipir is the only approved PET tracer compound for the visualisation of tau aggregation. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
High Aβ deposition (increased temporal [18F]-Flutemetamol standardized uptake value ratio (SUVr) and centiloid score), low glucose metabolism (decreased temporal lobe and posterior cingulate [18F]-FDG SUVr), low parietal CBF and right hemispheric cortical thickness were independent predictors of low cognitive test performance. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Shortening the amount of time required to acquire amyloid positron emission tomography (PET) brain images while maintaining the accuracy of quantitative evaluation would help to overcome motion artifacts associated with Alzheimer's disease patients. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The CAA and HTN-ICH groups had similar age (66.9 vs 67.1), sex, and leukoaraiosis volumes (31 vs 30 mL, all p > 0.8). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The following intersection over union values were obtained for the various slices in the verification dataset: frontal lobe axial/sagittal: 0.733/0.804; posterior cingulate cortex and precuneus coronal/sagittal: 0.661/0.726; lateral temporal lobe axial/coronal: 0.864/0.892; parietal lobe axial/coronal: 0.542/0.759; and striatum axial/sagittal: 0.679/0.752. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Florbetapir (18F) for brain amyloid positron emission tomography (PET) imaging has been recently approved in Europe to estimate β-amyloid neuritic plaque density in the brain when the subject is still alive. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The CL calculation was validated with the 18 F-florbetapir dataset in the GAAIN repository. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Until recently, estimation of β-amyloid plaque density as a key element for identifying Alzheimer's disease (AD) pathology as the cause of cognitive impairment was only possible at autopsy. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
When whole cerebellum or whole cerebellum plus brainstem was chosen as the reference area, an excellent correlation was found between the CL scale calculated by this software and the CL scale published by GAAIN. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Early diagnosis of mild cognitive impairment (MCI) fascinates screening high-risk Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
"Brain-predicted age" quantifies apparent brain age compared to normative neuroimaging trajectories. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Apathy severity was significantly associated with cortical thinning of the lateral parts of the right sided frontal, temporal and parietal lobes. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The microtubule-associated protein tau plays an important role in tauopathic diseases such as Alzheimer's disease and primary tauopathies such as progressive supranuclear palsy and corticobasal degeneration. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The SCD and aMCI groups showed both decreased ReHo in the right middle temporal gyrus (MTG) and decreased GMV compared to healthy controls (HCs). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The contribution of cerebellar pathology to cognitive and behavioural manifestations is increasingly recognised, but the cerebellar profiles of FTD phenotypes are relatively poorly characterised. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Identifying biomarkers of Alzheimer's disease (AD) will accelerate the understanding of its pathophysiology, facilitate screening and risk stratification, and aid in developing new therapies. 1 key finding →
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 →