27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
We used magnetic resonance imaging (MRI) measurements to determine whether persons in the prodromal phase of Alzheimer's disease (AD) could be accurately identified before they developed clinically diagnosed dementia. 1 key finding →
Participants: 24 Evidence: low
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Progressive CMRglc reductions on FDG-PET occur years in advance of clinical DAT symptoms in patients with pathologically verified disease. 1 key finding →
Design: longitudinal study Evidence: moderate
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These data support the use of rates of change from serial MRI studies in addition to standard clinical/psychometric measures as surrogate markers of disease progression in AD. 1 key finding →
Participants: 55 Evidence: low
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Assessment of the cingulum fibers using diffusion tensor imaging may aid early diagnosis of Alzheimer disease. 4 key findings →
Participants: 17 Evidence: low
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We compared the predictive value of cerebral perfusion as measured by arterial-spin labeling magnetic resonance imaging (ASL-MRI) with MRI-derived hippocampal volume for determining future cognitive and functional decline and subsequent conversion from mild cognitive impairment to dementia. 3 key findings →
Design: longitudinal study Evidence: moderate
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Rates of brain atrophy and/or ventricular enlargement were correlated with declining performance on cognitive scales. 2 key findings →
Design: longitudinal study Evidence: moderate
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Atrophy in FAD is observed early, both in areas commonly associated with sporadic Alzheimer disease and also in the putamen and thalamus, 2 regions associated with early amyloid deposition in FAD mutation carriers. 4 key findings →
Design: cross-sectional Participants: 192 Evidence: low
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The aim of this study was to assess the agreement between data on cerebral amyloidosis, derived using Pittsburgh compound B positron emission tomography and (i) multi-laboratory INNOTEST enzyme linked immunosorbent assay derived cerebrospinal fluid concentrations of amyloid-β42; (ii) centrally measured cerebrospinal fluid amyloid-β42 using a Meso Scale Discovery enzyme linked immunosorbent assay; and (iii) cerebrospinal fluid amyloid-β42 centrally measured using an antibody-independent mass spectrometry-based reference method. 3 key findings →
Participants: 243 Evidence: low
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The type, frequency, and extent of MR signal abnormalities in Alzheimer's disease and normal aging are a subject of controversy. 1 key finding →
Participants: 12 Evidence: low
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To accurately predict the development of Alzheimer's disease (AD) at its predementia stage would be a major breakthrough from both therapeutic and research standpoints. 5 key findings →
Design: longitudinal study Evidence: moderate
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Mutation carriers had significantly increased hippocampal and whole-brain atrophy rates compared with controls and these differences increased with time. 2 key findings →
Design: cross-sectional Evidence: moderate
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Our work shows that peripheral differential methylation between age-matched subjects with AD relative to healthy controls will provide opportunities to further investigate and validate differential methylation as a surrogate of disease. 2 key findings →
Design: longitudinal study Participants: 653 Evidence: moderate
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Alzheimer disease (AD) is primarily associated with accumulations of amyloid plaques and tau tangles in gray matter, however, it is now acknowledged that neuroinflammation, particularly in white matter (WM), significantly contributes to the development and progression of AD. 4 key findings →
Design: cross-sectional Participants: 310 Evidence: moderate
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Models of Alzheimer's disease (AD) pathophysiology posit that amyloidosis [A] precedes and accelerates tau pathology [T] that leads to neurodegeneration [N]. 4 key findings →
Design: longitudinal study Participants: 262 Evidence: moderate
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Measures are needed that identify persons that will develop Alzheimer's disease in order to target them for preventative interventions. 4 key findings →
Design: cross-sectional Participants: 20 Evidence: low
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Meta-analyses of epidemiological studies have suggested that Alzheimer's disease (AD) may be linked with exposure to extremely low frequency (ELF) magnetic fields (MF). 4 key findings →
Design: meta-analysis Participants: 155,562 Evidence: high
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Reduced hippocampal volume is a biomarker for neurodegeneration, but atrophy is not an AD-specific measure. 1 key finding →
Design: longitudinal study Evidence: moderate
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Amyloid PET results were positive for 242 patients (48%). 4 key findings →
Participants: 866 Evidence: moderate
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These observations suggest that brain amyloid deposition results in low CSF Abeta(42), and that amyloid imaging and CSF Abeta(42) may potentially serve as antecedent biomarkers of (preclinical) AD. 2 key findings →
Evidence: low
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We evaluated a new magnetic resonance (MR)-based technique for performing volumetric measurements of temporal lobe structures. 3 key findings →
Participants: 20 Evidence: low
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Individuals with an isolated pathologic diagnosis of AD, hippocampal sclerosis, frontotemporal degeneration, and neurofibrillary tangle--only degeneration usually had substantial hippocampal atrophy, while those with changes of typical aging did not. 2 key findings →
Participants: 67 Evidence: low
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Formation of senile plaques composed of amyloid beta peptide, a pathological hallmark of Alzheimer disease, in human brains precedes disease onset by many years. 2 key findings →
Design: longitudinal study Evidence: moderate
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ALPS-index may provide useful disease progression or treatment biomarkers for patients with AD as an indicator of modulation of glymphatic activity. 1 key finding →
Participants: 50 Evidence: low
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CA1 apical neuropil atrophy is apparent in patients with mild AD. 2 key findings →
Design: cross-sectional Participants: 14 Evidence: low
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10 of the 838 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 27,380 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 →