Of 386 participants, 199 (52%) were female, and the mean (SD) age was 68 (8) years. 3 key findings →
Design: cohort study Participants: 113 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Of 386 participants, 199 (52%) were female, and the mean (SD) age was 68 (8) years. 3 key findings →
Design: cohort study Participants: 113 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Reference region selection has an important influence on the detection of florbetapir change. 4 key findings →
Design: longitudinal study Participants: 14 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Our findings indicate that tau accumulates even in amyloid-negative healthy OA and this process can be measured with in vivo tau-PET. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Neuropathological and in vivo studies have revealed a tight relationship between tau pathology and cognitive impairment across the Alzheimer's disease spectrum. 5 key findings →
Participants: 40 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Although beta-amyloid (Abeta) plaques are a primary diagnostic criterion for Alzheimer's disease, this pathology is commonly observed in the brains of non-demented older individuals. 5 key findings →
Participants: 20 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Clinical phenotypes are associated with differential patterns of tau but not amyloid pathology. 3 key findings →
Participants: 119 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
β-Amyloid plaques and tau-containing neurofibrillary tangles are the two neuropathological hallmarks of Alzheimer's disease (AD) and are thought to play crucial roles in a neurodegenerative cascade leading to dementia. 2 key findings →
Design: longitudinal study Participants: 32 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The medial temporal lobe (MTL) is an early site of tau accumulation and MTL dysfunction may underlie episodic-memory decline in aging and dementia. 4 key findings →
Design: longitudinal study Participants: 83 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The goal of this paper was to evaluate the in vivo kinetics of the novel tau-specific PET radioligand 18 F-AV-1451 in cognitively healthy control (HC) and Alzheimer disease (AD) subjects, using reference region analyses. 2 key findings →
Design: longitudinal study Participants: 43 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The recent development of tau-specific positron emission tomography (PET) tracers enables in vivo quantification of regional tau pathology, one of the key lesions in Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
These findings suggest that patterns of cortical Aβ and tau do not differ in people with PD-CN, people with PD-MCI, and healthy older adults. 5 key findings →
Design: cross-sectional Participants: 30 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
[ 18 F]AV1451-PET and CSF p-tau had comparable value for differential diagnosis. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The correlation between white and gray matter disappeared after partial-volume correction in 11 C-PIB ( r 2 = 0) but persisted for 18 F-flortaucipir ( r 2 = 0.27), demonstrating that the correlation between white and gray matter signal in 18 F-flortaucipir is not solely due to partial-volume effects. 4 key findings →
Participants: 139 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The tau protein aggregates in aging and Alzheimer disease and may lead to memory loss through disruption of medial temporal lobe (MTL)-dependent memory systems. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
PET imaging with (11)C-labeled Pittsburgh Compound-B ((11)C-PIB) helps discriminate Alzheimer disease (AD) from frontotemporal lobar degeneration (FTLD). 2 key findings →
Participants: 12 Evidence: low
Full summary, score breakdown and related studies → Original source
Patients with early age-of-onset Alzheimer's disease show more rapid progression, more generalized cognitive deficits and greater cortical atrophy and hypometabolism compared to late-onset patients at a similar disease stage. 5 key findings →
Participants: 21 Evidence: low
Full summary, score breakdown and related studies → Original source
Determining the relative contribution of amyloid plaques and neurofibrillary tangles to brain dysfunction in Alzheimer disease is critical for therapeutic approaches, but until recently could only be assessed at autopsy. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Despite differing white and grey matter retention characteristics, cortical retention for each (18)F tracer was highly correlated with that of PiB, enabling conversion of thresholds across tracer measurement scales with a high level of internal consistency. 2 key findings →
Participants: 40 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
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
Normal aging is associated with a decline in episodic memory and also with aggregation of the β-amyloid (Aβ) and tau proteins and atrophy of medial temporal lobe (MTL) structures crucial to memory formation. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Although beta-amyloid (Aβ) deposition is a characteristic feature of Alzheimer's disease (AD), this pathology is commonly found in elderly normal controls (NC). 5 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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.
1,032 records (3.8% 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 →