30,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Ageing, a leading cause of the decline/deficits in human learning, memory, and cognitive abilities, is a major risk factor for age-associated neurodegenerative disorders such as Alzheimer’s disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The development of tau-specific positron emission tomography (PET) tracers allows imaging in vivo the regional load of tau pathology in Alzheimer's disease (AD) and other tauopathies. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tau PET was a significant mediator CBF/sPDGFRβ-MoCA relationships in numerous regions. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
The developed tau tracers show in silico and in vivo evidence of cross-interaction with MAO-B; the MAO-B component of the tracer binding was dependent on the regional concentration of the enzyme. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The aims of this study were: to examine regional rates of change in tau-PET uptake and grey matter volume in atypical Alzheimer's disease (AD); to investigate the role of age in such changes; to describe multimodal regional relationships between tau accumulation and atrophy. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tau and Aβ deposits in the elderly brain generally display well-defined hierarchical cortical relationships as well as overlaps between the principal clusters of both pathologic alterations in the heteromodal association regions. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Establishing the in vivo diagnosis of Alzheimer's disease (AD) or other dementias relies on clinical criteria; however, the accuracy of these criteria can be limited. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mildly elevated tau-PET binding was observed in a subset of amyloid-negative patients at risk for CTE, in a distribution consistent with CTE pathology stages III-IV. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
After applying PVC and controlling for age, education level and global cortical 18 F-AV-45 SUVR, we found that the entorhinal cortex, amygdala, parahippocampal gyrus, posterior cingulate, and occipital ROIs exhibited a significant ApoE ε4 by sex interaction effect (false discovery rate P < 0.1) among MCI individuals. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dementia, including Alzheimer's disease (AD), is a major disorder, leading to several ocular manifestations amongst the elderly population. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tau pathology was associated with locally reduced rCBF. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mild Behavioral Impairment (MBI) leverages later-life emergent and persistent neuropsychiatric symptoms (NPS) to identify a high-risk group for incident dementia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The results of this pilot study support a quantitative relationship between cortical flortaucipir SUVr values and quantitative measures of Ptau at autopsy. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Despite compelling evidence that the accumulation of amyloid-beta (Aβ) promotes neocortical MAPT (tau) aggregation in familial and idiopathic Alzheimer's disease (AD), murine models of cerebral amyloidosis are not considered to develop tau-associated pathology. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The participants presented here were clinically impaired, with structural imaging evidence of neurodegeneration, in the absence of any significant tau accumulation. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Molecular imaging of tauopathies is complicated by the differing specificities and off-target binding properties of available radioligands for positron emission tomography (PET). [ 18 F]-APN-1607 ([ 18 F]-PM-PBB3) is a newly developed PET tracer with promising properties for tau imaging. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Imaging of pathological tau with positron emission tomography (PET) has the potential to allow early diagnosis of the dementias and monitoring of disease progression, including assessment of therapeutic interventions, in vivo. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Heterogeneity within the Alzheimer's disease (AD) syndromic spectrum is typically classified in a domain-specific manner (e.g., language vs. visual cognitive function). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
LOnonAD subjects show a fronto-temporal neurodegenerative pattern in the absence of tau binding, which may represent underlying hippocampal sclerosis with TDP-43, also known as limbic-predominant age-related TDP-43 encephalopathy (LATE). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This research suggests different molecular targets for these tracers; while 11 C-PBB3 appeared to preferentially bind to tau deposits with a close spatial relationship to amyloid-beta, the binding pattern of 11 C-THK5351 fitted the expected distribution of tau pathology in Alzheimer's disease better and was more closely related to downstream disease markers. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
A strong correlation was found across different kinetic models ( R 2 > 0.97) and between DVR(2TC) and SUVR between 30 and 90 min, with an R 2 of more than 0.95. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
[ 18 F]MK-6240 is a selective, high-affinity PET radiotracer for imaging neurofibrillary tangles (NFT) in Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurodegenerative diseases characterized by pathological protein accumulation in cells are termed "proteinopathies." 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
See Kreisl (doi:10.1093/awx151) for a scientific commentary on this article. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
FBB, while having a narrower dynamic range than PiB, clearly distinguished HC from AD patients, with a comparable effect size. 1 key finding →
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 →