Alzheimer's disease (AD) is defined by amyloid (A) and tau (T) pathologies, with T better correlated to neurodegeneration (N). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
30,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Alzheimer's disease (AD) is defined by amyloid (A) and tau (T) pathologies, with T better correlated to neurodegeneration (N). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Similar to late-onset and autosomal dominant Alzheimer's disease (AD), high tau was an indicator of early prodromal AD in DS. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Visual assessment and semiquantitative analysis provide highly congruent results, thereby enhancing reader confidence and improving scan interpretation. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dual-phase amyloid PET is considered a useful protocol to study patients with cognitive impairment. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tau is one of several proteins associated with frontotemporal dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
APOE ε4 showed significant (P < .05) associations with tau deposition across all disease stages. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
SUVr calculated by our method and CortexID were highly correlated (R2 = 0.9657). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease-related atrophy in the posterior cingulate cortex, a key node of the default mode network, is present in the early stages of disease progression across clinical phenotypic variants of the disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Over the past decade, ocular imaging strategies have greatly advanced the diagnosis and follow-up of patients with optic neuropathies. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microglia are the resident macrophages of the central nervous system. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
These findings demonstrate that the aging gut microbiota drives detrimental changes in the gut-brain and gut-retina axes suggesting that microbial modulation may be of therapeutic benefit in preventing inflammation-related tissue decline in later life. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Corticobasal syndrome (CBS) is a clinical syndrome characterised by progressive asymmetric limb rigidity and apraxia with dystonia, myoclonus, cortical sensory loss and alien limb phenomenon. 3 key findings →
Design: narrative review Evidence: low
Full summary, score breakdown and related studies → Original source
The threshold for positivity was 15.085 pg/mL for plasma pTau181 and 17.652 pg/mL for plasma pTau231. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Next to amyloid and tau, synaptic loss is a key pathological hallmark in Alzheimer's disease, closely related to cognitive dysfunction and neurodegeneration. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The detection and staging of Alzheimer's disease (AD) using non-invasive imaging biomarkers is of substantial clinical importance. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Many neurodegenerative diseases are neuropathologically characterized by neuronal loss, gliosis, and the deposition of misfolded proteins such as β-amyloid (Aβ) plaques and tau tangles in Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is characterized by the presence of β-amyloid (Aβ) and tau, and subcortical vascular cognitive impairment (SVCI) is characterized by cerebral small vessel disease (CSVD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The extracellular buildup of amyloid beta (Aβ) plaques in the brain is a hallmark of Alzheimer's disease (AD). 2 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
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
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 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
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
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 30,180 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 30,180 records, built mostly from automated pulls of Europe PMC (64.2% of the library) and OpenAlex (16.9%), 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.
1,037 records (3.4% of the library) are not peer-reviewed — 964 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 →