Non-neurological surgery has both acute and long-term effects on the brain. 3 key findings →
Participants: 35 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Non-neurological surgery has both acute and long-term effects on the brain. 3 key findings →
Participants: 35 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Our data suggest that FXN ameliorates AD pathology, by simultaneously targeting two key pathological features: Aβ deposits and neuroinflammation. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The purpose is to review the latest advances of brain imaging for the diagnosis of Alzheimer disease (AD). 5 key findings →
Evidence: low
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Plasma ptau217 has strong diagnostic performance in distinguishing CSF biomarker-defined AD in a clinically relevant, younger cohort of people with symptoms, adding further weight for a simple diagnostic blood test for AD as a cause of a patient's symptoms. 2 key findings →
Evidence: moderate
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Frailty increasingly is recognized as a factor that modifies the relationship between disease biomarkers, including neuropathology, and dementia expression. 1 key finding →
Evidence: low
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Greater TSPO is associated with lower performance in episodic memory, attention/processing speed, executive function, language, and visuospatial ability in amyloid-positive individuals, but restricted to episodic memory in amyloid-negative individuals. 2 key findings →
Design: cross-sectional Participants: 21 Evidence: low
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Older age, White race, APOE ε4 carrier, and diabetes were associated with biomarker levels indicative of higher AD risk (lower Aβ42/40; higher p-tau217, p-tau217/Aβ42, NfL, and GFAP). 5 key findings →
Participants: 1,356 Evidence: low
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Among 871 participants (mean age: 62.80 ± 6.02 years), every SD increase in AIx and RI scores was both associated with 0.010 pg/mL (95% CI: 0.003–0.017, p = 0.004) higher blood p-tau217 levels after adjustment for age, employment status, BMI, mild cognitive impairment, hypertension, cholesterol-HDL ratio, renal function, and ApoE4 carrier status. 5 key findings →
Design: cross-sectional Participants: 871 Evidence: low
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Increased synthesis and release of S100 beta protein from activated astrocytes has been implicated in the overgrowth of dystrophic neurites in neuritic plaques in Alzheimer disease (AD). 4 key findings →
Evidence: low
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Deficits in glutamate neurotransmission and mitochondrial functions were detected in the frontal cortex (FC) and hippopcampus (HIPP) of aged 3×Tg-Alzheimer's disease (AD) mice, compared with their wild type littermates (non-Tg). 3 key findings →
Evidence: low
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The development of cerebrospinal fluid and blood-based biomarkers for Alzheimer disease (AD) and related disorders is rapidly progressing. 5 key findings →
Evidence: low
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Hepatocyte growth factor (HGF/SF), is a heparin-binding polypeptide which stimulates DNA synthesis in a variety of cell types and also promotes cell migration and morphogenesis. 4 key findings →
Evidence: low
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Glial fibrillary acidic protein (GFAP) is the structural protein of the astroglial intermediate filament that forms the morphological basis of astrogliosis. 2 key findings →
Participants: 39 Evidence: low
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It is well known that a specific set of genetic and non-genetic risk factors contributes to the onset of Alzheimer disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease is a severe neurodegenerative disorder of the brain, pathologically characterized by extracellular beta-amyloid plaques, intraneuronal Tau inclusions, inflammation, reactive glial cells, vascular pathology and neuronal cell death. 1 key finding →
Evidence: low
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We conclude that an inverse correlation between levels of inflammation in cortical areas and plasma NfL levels indicates that microglial activation may initially be protective to axons in AD. 3 key findings →
Evidence: low
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Positron emission tomography (PET) imaging of brain amyloid beta is now clinically available in several countries including the United States and the United Kingdom, but not Canada. 1 key finding →
Evidence: low
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The human GFAP splice variants GFAPDelta164 and GFAPDeltaexon6 both result in a GFAP protein isoform with a unique out-of-frame carboxy-terminus that can be detected by the GFAP+1 antibody. 3 key findings →
Evidence: low
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Alzheimer's disease (AD) is the most common neurodegenerative disorder that leads to progressive cognitive decline and imposes a significant socio-economic burden. 1 key finding →
Evidence: low
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The associations of lower foveal capillary density with cerebral WMH and amyloid positivity suggest that further research is warranted to evaluate for shared mechanisms of disease between small vessel disease and AD pathologies. 5 key findings →
Participants: 41 Evidence: low
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Prior work on the link between blood-based biomarkers and cognitive status has largely been based on dichotomous classifications rather than detailed neuropsychological functioning. 1 key finding →
Participants: 395 Evidence: low
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We question the validity of the evidence for the removal of amyloid in particular as assessed by amyloid PET imaging, believing that what is observed is more likely a large nonspecific amyloid PET signal in the white matter that diminishes during immunotherapy-in line with dose-dependent increases in amyloid-related imaging abnormalities and increased loss of cerebral volume in treated compared with placebo patients. 1 key finding →
Evidence: low
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Quantification of in vivo amyloid and tau PET imaging relationships with postmortem measurements are critical for validating the sensitivity and specificity imaging biomarkers across clinical phenotypes with Alzheimer disease neuropathologic change (ADNC). 3 key findings →
Evidence: low
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Among CU participants, men had lower Aβ42 and GFAP, and higher p-tau217/Aβ42. 5 key findings →
Evidence: low
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Plasma biomarkers demonstrate promise for improving diagnostic accuracy in diverse research cohorts. 3 key findings →
Evidence: moderate
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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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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 →