27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
In our study, TSH was related neither to risk of AD nor with early MRI markers thereof, arguing against an important role of thyroid function in the development of AD. 4 key findings →
Design: cohort study Participants: 1,025 Evidence: moderate
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Three women (aged 61, 72, and 73 years) consecutively enrolled in the trial successfully completed repeated focused ultrasound-induced BBB opening of the hippocampus and entorhinal cortex. 1 key finding →
Evidence: low
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There were detectable WMH, enlarged PVS, infarcts, and microbleeds as early as the 5th decade of life. 2 key findings →
Design: cross-sectional Participants: 138 Evidence: low
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Although white matter hyperintensities have traditionally been viewed as a marker of vascular disease, recent pathology studies have found an association between white matter hyperintensities and Alzheimer's disease pathologies. 4 key findings →
Participants: 434 Evidence: low
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Clinical data alone poorly predicted phenoconversion in RBD due to synucleinopathy patients. 3 key findings →
Participants: 173 Evidence: low
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Empathy is a complex social behaviour mediated by a network of brain structures. 3 key findings →
Participants: 123 Evidence: low
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To design clinical trials for the frontotemporal lobar degenerations (FTLD), knowledge about measurement of disease progression is needed to estimate power and enable the choice of optimal outcome measures. 2 key findings →
Participants: 107 Evidence: low
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SEE THAL AND VANDENBERGHE DOI101093/BRAIN/AWW057 FOR A SCIENTIFIC COMMENTARY ON THIS ARTICLE: Post-mortem Braak staging of neurofibrillary tau tangle topographical distribution is one of the core neuropathological criteria for the diagnosis of Alzheimer's disease. 1 key finding →
Participants: 14 Evidence: low
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Cerebrospinal fluid and positron emission tomography amyloid-β were measured at baseline in 769 persons [161 healthy controls, 68 subjective memory complaints, 419 mild cognitive impairment and 121 Alzheimer's disease dementia, mean age 72 years (standard deviation 7 years), 47% females] and used to predict diagnosis, APOE ε4 carriage status, cerebral blood flow, cerebrospinal fluid total-tau and phosphorylated-tau levels (cross-sectionally); and hippocampal volume, fluorodeoxyglucose positron emission tomography results and Alzheimer's Disease Assessment Scale-cognitive subscale scores (longitudinally). 2 key findings →
Participants: 769 Evidence: low
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Accurate prediction of clinical changes of mild cognitive impairment (MCI) patients, including both qualitative change (i.e., conversion to Alzheimer's disease (AD)) and quantitative change (i.e., cognitive scores) at future time points, is important for early diagnosis of AD and for monitoring the disease progression. 1 key finding →
Design: longitudinal study Evidence: moderate
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The fornix is a predominant outflow tract of the hippocampus and may be an important indicator of AD progression. 2 key findings →
Design: cross-sectional Participants: 75 Evidence: moderate
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Physical and cognitive exercise may prevent or delay dementia in later life but the neural mechanisms underlying these therapeutic benefits are largely unknown. 3 key findings →
Participants: 100 Evidence: low
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The sensitivity of MRI volumetric measures to detect cognitive dysfunction is examined in 39 participants of an epidemiological field study (age 75-85, MMSE 19-30). 4 key findings →
Participants: 39 Evidence: low
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The gap between predicted brain age using magnetic resonance imaging (MRI) and chronological age may serve as a biomarker for early-stage neurodegeneration. 4 key findings →
Design: longitudinal study Evidence: moderate
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Apolipoprotein (APOE) e4 genotype is an accepted risk factor for accelerated cognitive aging and dementia, though its neurostructural substrates are unclear. 4 key findings →
Design: cross-sectional Participants: 8,395 Evidence: moderate
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Total tau protein (T-Tau) and neurofilament light chain (NfL) have emerged as candidate plasma biomarkers of neurodegeneration, but studies have not compared how these biomarkers cross-sectionally or longitudinally associate with cognitive and neuroimaging measures. 4 key findings →
Design: cross-sectional Participants: 995 Evidence: moderate
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Medical imaging provides numerous insights into the subclinical changes that precede serious diseases such as heart disease and dementia. 4 key findings →
Design: cross-sectional Evidence: low
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The reference standard for amyloid-PET quantification requires structural MRI (sMRI) for preprocessing in both multi-site research studies and clinical trials. 4 key findings →
Participants: 740 Evidence: low
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We analyzed data from 462 ADNI participants without dementia who underwent Aβ ([ 18 F]florbetapir or [ 18 F]florbetaben) and tau ([ 18 F]flortaucipir) PET, structural MRI, and cognitive testing. 4 key findings →
Design: cross-sectional Participants: 156 Evidence: moderate
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There is a growing literature on the importance of hippocampal volume in geriatric depression. 4 key findings →
Design: longitudinal study Participants: 66 Evidence: moderate
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Braak stages of tau neurofibrillary tangle accumulation have been incorporated in the criteria for the neuropathological diagnosis of Alzheimer's disease. 4 key findings →
Participants: 301 Evidence: low
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's ≥ 0.75). Both markers identified Braak stage V-VI levels with similarly high performance (entorhinal SUVR, area under the curve [AUC] = 0.92 [95% CI 0.91-0.93]; temporal meta-ROI SUVR, AUC = 0.91 [95% CI 0.90-0.92]; plasma p-tau217, AUC = 0.90 [95% CI 0.89-0.91]), but PET outperformed plasma p-tau217 in identifying high/intermediate ADNCs (entorhinal ROI, AUC = 0.94 [95% CI 0.94-0.95]; temporal meta-ROI AUC = 0.94 [95% CI 0.94-0.95]; plasma p-tau217, AUC = 0.89 [95% CI 0.88-0.90]). 2 key findings →
Participants: 56 Evidence: moderate
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(69.4% female) were aged 68.3 ± 5.1 years at their first PET scans. 5 key findings →
Design: longitudinal study Participants: 243 Evidence: moderate
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-fold changes of 1.21, 0.57, and 4.63, respectively, compared to A-. 5 key findings →
Design: cross-sectional Participants: 252 Evidence: low
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The discovery cohort contained 3,671 individuals with a mean age of 68 years and consisted of 49% reported female. 5 key findings →
Participants: 3,671 Evidence: moderate
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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 →