Both FC-BAG and S-BAG are elevated in CI participants. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Research
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Future studies should emphasize collection of relevant psychosocial factors in addition to the development of intentional diversity and inclusion efforts to improve the racial/ethnic and socioeconomic representativeness of AD studies. 1 key finding →
Participants: 131 Evidence: low
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Though it is not without inherent challenges, fNIRS may have advantages over other neuroimaging techniques in the areas of speech and language impairment. fNIRS has clinical applications that may lead to improved early and differential diagnosis, increase our understanding of response to treatment, improve neuroprosthetic functioning, and advance neurofeedback. 1 key finding →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
According to the World Health Organization (WHO), dementia is the seventh leading reason of death among all illnesses and one of the leading causes of disability among the world's elderly people. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Compared to controls, mean CSF NPTX2 levels were lower in DS at all AD stages; aDS (0.6-fold, adj.p 0.07). 2 key findings →
Design: cross-sectional Participants: 49 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
High-dimensional pattern classification was applied to baseline and multiple follow-up MRI scans of the Alzheimer's Disease Neuroimaging Initiative (ADNI) participants with mild cognitive impairment (MCI), in order to investigate the potential of predicting short-term conversion to Alzheimer's Disease (AD) on an individual basis. 1 key finding →
Evidence: low
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Semiautomated, individually specific quantitative MR imaging methods can be used to identify a pattern of regional atrophy in MCI that is predictive of clinical decline. 2 key findings →
Participants: 84 Evidence: low
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[(11)C]PIB retention in the neocortical and subcortical brain regions was significantly higher in AD patients than in age-matched controls. 3 key findings →
Participants: 97 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Cognitive decline is one of the most frequent and disabling nonmotor features of Parkinson's disease. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
53/100
Baseline brain volume was lowest in AD but did not differ significantly between MCI, subjective complaints, and control groups (P > .38). 3 key findings →
Participants: 65 Evidence: low
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The hippocampus is the brain structure of highest and earliest structural alteration in Alzheimer's disease (AD). 4 key findings →
Design: longitudinal study Evidence: moderate
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The two primary molecular pathologies in Alzheimer's disease are amyloid-β plaques and tau-immunoreactive neurofibrillary tangles. 4 key findings →
Evidence: moderate
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Cross-sectional data, including CSF analytes, molecular imaging of cerebral fibrillar β-amyloid (Aβ) with PET using the [ 11 C] benzothiazole tracer Pittsburgh compound B (PiB), MRI-based brain structures, and clinical/cognitive outcomes harmonized from 8 studies, collectively involving 3,284 cognitively normal individuals 18 to 101 years of age, were analyzed. 4 key findings →
Design: cross-sectional Evidence: low
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53/100
This prospective, observational study enrolled patients with early AD undergoing Alzheimer's biomarker analysis and matched controls. 4 key findings →
Design: longitudinal study Participants: 15 Evidence: moderate
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White matter hyperintensities (WMH) correlate with Alzheimer disease (AD) biomarkers cross-sectionally and modulate AD pathogenesis. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
ARIA monitoring is important to inform treatment dosing decisions and might be improved through assistive software. 4 key findings →
Participants: 16 Evidence: low
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Early identification of dementia at the stage of mild cognitive impairment (MCI) is crucial for timely diagnosis and intervention of Alzheimer's disease (AD). 4 key findings →
Participants: 174 Evidence: low
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Predicting the progression of cognitive decline in Alzheimer's disease (AD) is important for treatment selection and patient counseling. 4 key findings →
Participants: 124 Evidence: moderate
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Activated microglia may play a role in the pathogenesis of Alzheimer disease (AD) as they cluster around beta-amyloid (Abeta) plaques. 4 key findings →
Evidence: low
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For amyloid positive individuals Aβ42/Aβ40, glial fibrillary acidic protein and p-tau181 were the top predictors of cognitive decline while Aβ42/Aβ40 was prominent for amyloid negative participants across all age groups. 5 key findings →
Design: cross-sectional Participants: 1,185 Evidence: moderate
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Greater intra-group heterogeneity in ATN abnormality patterns was observed in more severe clinical stages of AD. 5 key findings →
Design: cross-sectional Participants: 665 Evidence: low
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Pathophysiologic-constrained ADL provided interpretable, personalized pathologic maps and an AI-derived ADAD score that more closely linked PET pathologic abnormalities with multimodal clinical measures. © RSNA, 2026 3 key findings →
Design: longitudinal study Participants: 7,457 Evidence: moderate
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Midlife individuals who experienced HDP had lower regional CBF and reduced white matter microstructural integrity, compared with those with no adverse pregnancy outcomes. 5 key findings →
Design: prospective cohort Participants: 81 Evidence: moderate
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The final model, which included age, systolic blood pressure >140, atrial fibrillation, and tobacco use, achieved an AUC of 0.83 (95% CI 0.75-0.90) in the development cohort (N=143, 62.4±12.6 years, 44% female, 36% non-white race) and 0.85 (95% CI 0.77-0.92) in the validation cohort (N=127, 65.2±16.8 years, 51% female, 34% non-white race), with similar results using WMH measurements derived from cMRI (N=120, p=0.98, AUC=0.86, 95% CI 0.77-0.93). 5 key findings →
Participants: 143 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
We conclude that PiB-positron emission tomography can detect cerebrovascular beta-amyloid and may serve as a method for identifying the extent of CAA in living subjects.
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From across this tag
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.
- Tau: From research to clinical development
- Comparison of amyloid PET acquired through standardized and unstandardized protocols
- Vascular risk and Aβ interact to reduce cortical thickness in AD vulnerable brain regions
- Morphometric and histologic substrates of cingulate integrity in elders with exceptional memory capacity
- Development and Validation of a 18 F-Flortaucipir PET Visual Stratification Method
- MRI and CSF biomarkers in normal, MCI, and AD subjects: predicting future clinical change
- Amyloid-Related Imaging Abnormalities and Other MRI Findings in a Cognitively Unimpaired Population With and Without Cerebral Amyloid
- Plasma P-tau181 to Aβ42 ratio is associated with brain amyloid burden and hippocampal atrophy in an Asian cohort of Alzheimer's disease patients with concomitant cerebrovascular disease
- Defining imaging biomarker cut points for brain aging and Alzheimer's disease
- Independent comparison of CogState computerized testing and a standard cognitive battery with neuroimaging
Where “Free full text” comes from
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
How the 0–100 score works — and why some entries are capped
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.
- Journal tier up to 10 pts
- Journal's citation record up to 4 pts
- Study design up to 12 pts
- Strength of evidence up to 5 pts
- Peer-review validation up to 10 pts
- How recent up to 5 pts
- Sample size up to 4 pts
- Effect reported up to 3 pts
- Studied in people up to 3 pts
- Randomised / blinded up to 2 pts
- Times cited up to 7 pts
- Citations per year up to 5 pts
- Impact for its field and year up to 6 pts
- Cited by studies here up to 6 pts
- Still being cited up to 4 pts
- Senior author's track record up to 4 pts
- Institution's track record up to 3 pts
- Multi-centre collaboration up to 3 pts
- Indexed in PubMed up to 2 pts
- Free to read up to 2 pts
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.
What this library is — and isn't
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 →