Twenty patients with AD and 25 CN subjects had MRI scans and clinical evaluations twice approximately 1.9 years apart. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Twenty patients with AD and 25 CN subjects had MRI scans and clinical evaluations twice approximately 1.9 years apart. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
WMC severity and diabetes are independent predictors of cognitive decline in an initially nondisabled elderly population. 1 key finding →
Participants: 639 Evidence: low
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SVaD without abnormal amyloid imaging was more common than expected. 4 key findings →
Participants: 45 Evidence: low
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[ 18 F]AV1451-PET and CSF p-tau had comparable value for differential diagnosis. 4 key findings →
Evidence: low
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In both patient groups, intrinsic connectivity between hippocampus and precuneus was significantly reduced. 3 key findings →
Participants: 21 Evidence: low
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The double dissociation in performance on semantic memory and attention/executive function clearly separated the temporal and frontal variants of FTD and aids the early differentiation of FTD from AD. 3 key findings →
Evidence: low
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Incorporating quantitative assessment of learning ability along with vMRI or CSF biomarkers in the clinical workup of MCI can provide critical information on risk of imminent conversion to AD. 3 key findings →
Evidence: low
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Rates of atrophy accelerate as individuals progress from amnestic mild cognitive impairment (aMCI) to typical late onset Alzheimer disease (AD). 1 key finding →
Participants: 46 Evidence: low
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We found no evidence of acceleration in whole-brain atrophy rates in any group. 1 key finding →
Evidence: low
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Increased Aβ burden was observed in TBI. 2 key findings →
Evidence: low
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Structural brain changes in anatomic areas involved in higher cognitive processes precede clinical signs and symptoms in longitudinally followed normal subjects destined to develop mild cognitive impairment. 1 key finding →
Participants: 23 Evidence: low
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Callosal changes are already present in patients with amnestic mild cognitive impairment (MCI) and mild Alzheimer disease (AD). 3 key findings →
Participants: 38 Evidence: low
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A temporoparietal pattern of atrophy on MRI in patients with progressive fluent aphasia and relatively preserved processing speed is suggestive of underlying Alzheimer disease pathology rather than frontotemporal lobar degeneration with ubiquitin-only immunoreactive changes. 3 key findings →
Participants: 216 Evidence: low
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Disease-specific patterns of functional network topology and connectivity alterations were observed in patients with EOAD and bvFTD. 3 key findings →
Participants: 37 Evidence: low
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The AS task is a useful measure of executive function across the AD spectrum. 1 key finding →
Participants: 182 Evidence: low
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The long-chain ω-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are potential candidates for interventions to delay Alzheimer disease (AD), but evidence from clinical studies is mixed. 1 key finding →
Participants: 281 Evidence: low
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None of the clinical criteria for VaD identified the same group of subjects. 2 key findings →
Participants: 52 Evidence: low
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Neither PPA phenotyping nor imaging alone is a reliable predictor of pathology. 4 key findings →
Participants: 19 Evidence: low
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= 0.008). Deficits in medial temporal CVR are observed in older adults with MCI and are related to worse memory function. 4 key findings →
Design: cross-sectional Evidence: moderate
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Rates of hippocampal atrophy match both baseline cognitive status and the change in cognitive status over time in elderly persons who lie along the cognitive continuum from normal to MCI to AD.
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PiB and FDG showed similar accuracy in discriminating AD and FTLD. 2 key findings →
Participants: 62 Evidence: low
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[18F]Flortaucipir BPND images showed overall highest binding in the symptomatic carriers. 5 key findings →
Participants: 52 Evidence: low
Full summary, score breakdown and related studies → Original source
The regions of loss observed in subjects with amnestic mild cognitive impairment (aMCI) who progressed to Alzheimer disease (AD) within 18 months of the MRI are typical of subjects with AD. 3 key findings →
Evidence: low
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Revised diagnostic criteria for Alzheimer disease (AD) acknowledge a key role of imaging biomarkers for early diagnosis. 5 key findings →
Evidence: low
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Alzheimer disease (AD) and, to a lesser extent, dementia with Lewy bodies (DLB) showed more pronounced MTA. 3 key findings →
Participants: 39 Evidence: low
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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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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 (3.6% 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 →