76/100
✓ Peer-reviewed
alzhub usefulness score 76 out of 100.
·
JAMA neurology
·
2019-07-01
The NfL level was increased at baseline in patients with mild cognitive impairment and AD dementia (mean levels: cognitive unimpairment, 32.1 ng/L; mild cognitive impairment, 37.9 ng/L; and AD dementia, 45.9 ng/L; P Conclusions and relevance The findings suggest that plasma NfL can be used as a noninvasive biomarker associated with neurodegeneration in patients with AD and may be useful to monitor effects in trials of disease-modifying drugs. 3 key findings →
Design: cohort study
Participants: 1,583
Evidence: moderate
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75/100
✓ Peer-reviewed
alzhub usefulness score 75 out of 100.
·
JAMA neurology
·
2017-05-01
Among 193 cognitively healthy controls, 197 patients with mild cognitive impairment, and 180 patients with AD with dementia, plasma NFL correlated with CSF NFL (Spearman ρ = 0.59, P Conclusions and relevance Plasma NFL is associated with AD diagnosis and with cognitive, biochemical, and imaging hallmarks of the disease. 3 key findings →
Design: case-control study
Participants: 197
Evidence: moderate
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70/100
✓ Peer-reviewed
alzhub usefulness score 70 out of 100.
·
Neurology
·
2017-12-01
Increased levels of triglycerides at midlife predict brain Aβ and tau pathology 20 years later in cognitively healthy individuals. 5 key findings →
Design: cohort study
Participants: 134
Evidence: moderate
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Baseline plasma GFAP could detect abnormal CSF Aβ42/40 and CSF Aβ42/T-tau with an AUC of 0.79 (95% CI 0.72-0.86) and 0.80 (95% CI 0.72-0.86), respectively. 3 key findings →
Design: longitudinal study
Evidence: moderate
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66/100
✓ Peer-reviewed
alzhub usefulness score 66 out of 100.
·
Neurology
·
2016-01-29
An optimized immunoassay was used to analyze CSF Ng in a retrospective cohort of 331 participants with different neurodegenerative diseases, including healthy controls (n = 19), biomarker-proven Alzheimer disease (AD) (n = 100), genetic AD (n = 2), behavioral variant frontotemporal dementia (n = 20), speech variant frontotemporal dementia (n = 21), Lewy body dementia (n = 13), Parkinson disease (n = 31), progressive supranuclear palsy (n = 46), multiple system atrophy (n = 29), as well as a heterogeneous group with non-neurodegenerative cognitive impairment (n = 50). 1 key finding →
Design: retrospective cohort
Participants: 19
Evidence: moderate
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63/100
✓ Peer-reviewed
alzhub usefulness score 63 out of 100.
·
Neurology
·
2017-07-05
Self-report of poor sleep was associated with greater AD-related pathology in cognitively healthy adults at risk for AD. 3 key findings →
Participants: 101
Evidence: moderate
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A tau/Aβ42 ratio of >0.52 constitutes a robust cerebrospinal fluid Alzheimer profile. 3 key findings →
Participants: 1,442
Evidence: moderate
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60/100
✓ Peer-reviewed
alzhub usefulness score 60 out of 100.
·
JAMA network open
·
2023-11-01
These findings suggest that increases in certain plasma AD biomarkers are associated with NP in WLWH and WLWOH and may be associated with later onset of AD, and measuring these biomarkers could be a pivotal advancement in monitoring aging brain health and development of AD among women with and without HIV. 5 key findings →
Design: cohort study
Participants: 307
Evidence: moderate
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The discovery that heterozygous missense mutations in the gene encoding triggering receptor expressed on myeloid cells 2 (TREM2) are risk factors for Alzheimer's disease (AD), with only the apolipoprotein E (APOE) ε4 gene allele conferring a higher risk, has led to increased interest in immune biology in the brain. 4 key findings →
Participants: 37
Evidence: moderate
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Widespread implementation of cerebrospinal fluid (CSF) biomarkers of Alzheimer's disease (AD) in clinical settings requires improved accuracy for diagnosis of prodromal disease and for distinguishing AD from non-AD dementias. 4 key findings →
Participants: 338
Evidence: moderate
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56/100
✓ Peer-reviewed
alzhub usefulness score 56 out of 100.
·
PloS one
·
2022-05-26
Two genetic variants in strong linkage disequilibrium (rs9536314 and rs9527025) in the Klotho (KL) gene, encoding a transmembrane protein, implicated in longevity and associated with brain resilience during normal aging, were recently shown to be associated with Alzheimer disease (AD) risk in cognitively normal participants who are APOE ε4 carriers. 4 key findings →
Participants: 5,541
Evidence: low
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55/100
✓ Peer-reviewed
alzhub usefulness score 55 out of 100.
·
Neurology
·
2018-06-29
These results provide evidence that, in the absence of significant neurodegenerative processes, individuals who harbor AD neuropathology may remain cognitively unimpaired. 4 key findings →
Design: cross-sectional
Participants: 79
Evidence: low
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55/100
✓ Peer-reviewed
alzhub usefulness score 55 out of 100.
·
Neurology
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2016-04-15
Amyloid-positive cognitively healthy participants showed a significant increase in mI/creatine and mI/NAA levels compared to amyloid-negative healthy elderly (p Conclusions mI levels are elevated already at asymptomatic stages of AD. 2 key findings →
Design: cross-sectional
Evidence: low
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53/100
✓ Peer-reviewed
alzhub usefulness score 53 out of 100.
·
Neurology
·
2017-03-24
Ninety-five individuals from the Wisconsin Registry for Alzheimer's Prevention were included in these cross-sectional analyses. 4 key findings →
Design: cross-sectional
Evidence: moderate
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In vitro and animal studies have suggested that inoculation with herpes simplex virus 1 (HSV-1) can lead to amyloid deposits, hyperphosphorylation of tau, and/or neuronal loss. 4 key findings →
Participants: 58
Evidence: low
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52/100
✓ Peer-reviewed
alzhub usefulness score 52 out of 100.
·
JAMA network open
·
2026-07-01
In vivo biomarkers for detecting neuropathologies from repetitive head impacts (RHI), including chronic traumatic encephalopathy (CTE), are needed. 4 key findings →
Design: case-control study
Participants: 231
Evidence: moderate
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Rare variants should only be investigated in users with a family history of early-onset dementia in a first degree relative. 5 key findings →
Evidence: low
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It is unknown whether multidomain interventions, which might preserve late-life cognition, affect Alzheimer's disease pathology. 4 key findings →
Participants: 527
Evidence: high
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There is a need for an accessible biomarker that can complement current cerebrospinal fluid and imaging biomarkers in an accurate and early diagnosis of Alzheimer disease (AD). 4 key findings →
Evidence: low
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The search for accessible and cost-effective biomarkers to complement current cerebrospinal fluid (CSF) and imaging biomarkers in the accurate detection of Alzheimer disease (AD) and other common neurodegenerative disorders remains a challenging task. 5 key findings →
Evidence: low
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45/100
✓ Peer-reviewed
alzhub usefulness score 45 out of 100.
·
PloS one
·
2015-05-08
The purpose of the present study was to investigate if cerebrospinal fluid (CSF) biomarkers of neurodegeneration are associated with cognition in bipolar disorder and healthy controls, respectively. 4 key findings →
Evidence: low
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Alzheimer disease (AD) is characterized by amyloid-β plaques (A), tau tangles (T), and neurodegeneration (N), collectively defining the ATN framework. 4 key findings →
Design: longitudinal study
Evidence: moderate
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The association between an AD-like signature using the established biomarkers Aβ42, T-tau, and P-tau with increased levels of NFL provides in vivo evidence of an association between AD and subcortical axonal degeneration in this uniquely large dataset of CSF samples tested for dementia biomarkers. 2 key findings →
Evidence: low
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Non-neurological surgery has both acute and long-term effects on the brain. 3 key findings →
Participants: 35
Evidence: low
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42/100
✓ Peer-reviewed
alzhub usefulness score 42 out of 100.
·
Stem cell reports
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2017-03-09
Human stem cell models have the potential to provide platforms for phenotypic screens to identify candidate treatments and cellular pathways involved in the pathogenesis of neurodegenerative disorders. 1 key finding →
Evidence: low
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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
- Randomized / 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
- Multicenter 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 31,380 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.