The core biomarkers differentiated Alzheimer's disease from controls with good performance: CSF T-tau (average ratio 2·54, 95% CI 2·44-2·64, p Interpretation The core CSF biomarkers of neurodegeneration (T-tau, P-tau, and Aβ42), CSF NFL, and plasma T-tau were strongly associated with Alzheimer's disease and the core biomarkers were strongly associated with mild cognitive impairment due to Alzheimer's disease. 2 key findings →
Design: systematic review
Participants: 699
Evidence: high
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76/100
✓ Peer-reviewed
alzhub usefulness score 76 out of 100.
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JAMA neurology
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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.
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JAMA neurology
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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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74/100
✓ Peer-reviewed
alzhub usefulness score 74 out of 100.
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Neurology
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2016-09-30
Plasma tau partly reflects AD pathology, but the overlap between normal aging and AD is large, especially in patients without dementia. 3 key findings →
Design: longitudinal study
Participants: 179
Evidence: moderate
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71/100
✓ Peer-reviewed
alzhub usefulness score 71 out of 100.
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Neurology
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2018-04-13
The prevalence of pathologic AD markers was very common (46%) in a representative population sample of 70-year-olds. 3 key findings →
Design: cohort study
Participants: 322
Evidence: moderate
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69/100
✓ Peer-reviewed
alzhub usefulness score 69 out of 100.
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JAMA neurology
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2019-09-01
These data support the use of cNfL as a biomarker of neuroaxonal damage and indicate that age-specific and sex-specific (and in some cases disease-specific) reference values may be needed. 4 key findings →
Participants: 2,795
Evidence: moderate
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Plasma p-tau217 showed larger fold-changes and better accuracy for detecting AD pathology in symptomatic individuals, with greater cross-platform agreement than other p-tau variants. 2 key findings →
Design: case-control study
Participants: 40
Evidence: moderate
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68/100
✓ Peer-reviewed
alzhub usefulness score 68 out of 100.
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JAMA neurology
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2019-03-01
Cognitive testing follow-up occurred for 1 to 18 years (mean [SD], 0.98 [2.25] years); autopsy-verified diagnoses were available for 120 of 845 participants with diseases (14.2%). 2 key findings →
Design: case-control study
Participants: 913
Evidence: moderate
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66/100
✓ Peer-reviewed
alzhub usefulness score 66 out of 100.
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JAMA neurology
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2014-10-01
The agreement between Aβ classification with CSF Aβ42 and 18F-flutemetamol positron emission tomography was very high (κ = 0.85). 3 key findings →
Design: cross-sectional
Participants: 118
Evidence: moderate
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Cerebrospinal fluid neurogranin was increased in patients with Alzheimer's disease dementia (P < 0.001), progressive mild cognitive impairment (P < 0.001) and stable mild cognitive impairment (P < 0.05) compared with controls, and in Alzheimer's disease dementia (P < 0.01) and progressive mild cognitive impairment (P < 0.05) compared with stable mild cognitive impairment. 2 key findings →
Design: longitudinal study
Participants: 95
Evidence: moderate
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CSF Aβ levels are altered in a subset of patients with early PD and relate to memory impairment. 4 key findings →
Design: longitudinal study
Participants: 20
Evidence: moderate
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We used a sensitive and specific beta-site amyloid precursor protein (APP)-cleaving enzyme 1 (BACE1) assay to determine the relationship between BACE1 activity in cerebrospinal fluid (CSF) and markers of APP metabolism and axonal degeneration in early and late stages of Alzheimer disease (AD). 4 key findings →
Design: case-control study
Participants: 113
Evidence: moderate
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Ascertainment of the -synuclein level in CSF somewhat improves the differential diagnosis of AD vs DLB and PDD when combined with established AD biomarkers. 3 key findings →
Design: cross-sectional
Participants: 453
Evidence: low
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A growing body of evidence suggests that the plasma concentration of the neurofilament light chain (NfL) might be considered a plasma biomarker for the screening of neurodegeneration in Alzheimer's disease (AD). 4 key findings →
Participants: 25
Evidence: low
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57/100
✓ Peer-reviewed
alzhub usefulness score 57 out of 100.
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JAMA psychiatry
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2014-10-01
The CSF levels of Aβ42 but not total and phosphorylated tau were lower in APOE ε4 carriers compared with noncarriers irrespective of diagnostic group (cohort A). 3 key findings →
Participants: 105
Evidence: moderate
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The NTK contains promising markers that improve the pathophysiological characterization of AD. 1 key finding →
Participants: 720
Evidence: low
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Galectin-3 (Gal-3) is a beta-galactosidase binding protein involved in microglial activation in the central nervous system (CNS). 5 key findings →
Participants: 119
Evidence: low
Full summary, score breakdown and related studies →
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Neurogranin (Ng) is a post-synaptic protein that previously has been shown to be a biomarker for synaptic function when measured in cerebrospinal fluid (CSF). 5 key findings →
Participants: 915
Evidence: low
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53/100
✓ Peer-reviewed
alzhub usefulness score 53 out of 100.
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Neurology
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2014-04-18
These in vivo data support the role of Aβ pathology in the etiology and highlight the potential utility of CSF Aβ42 as an early prognostic biomarker of dementia associated with PD. 3 key findings →
Participants: 20
Evidence: moderate
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CSF Abeta1-14, Abeta1-15, and Abeta1-16 increase during gamma-secretase inhibitor treatment in AD, even at doses that do not affect Abeta1-42 or Abeta1-40, probably because of increased substrate availability of the C99 APP stub (APP beta-CTF) induced by gamma-secretase inhibition. 2 key findings →
Participants: 35
Evidence: high
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Neuroinflammation and synaptic degeneration are major neuropathological hallmarks in Alzheimer's disease (AD). 3 key findings →
Participants: 95
Evidence: low
Full summary, score breakdown and related studies →
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Molecular subtypes of sporadic CJD show different levels of plasma tau. 2 key findings →
Participants: 132
Evidence: low
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Alzheimer's disease (AD) and vascular dementia (VaD) are intertwined by mixed dementia (MD) harboring varying degrees of AD pathology in combination with cerebrovascular disease. 5 key findings →
Participants: 30
Evidence: low
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47/100
✓ Peer-reviewed
alzhub usefulness score 47 out of 100.
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EBioMedicine
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2015-11-22
Plasma and CSF NFL concentrations were very highly correlated (r = 0.89, P < 0.0001). 1 key finding →
Design: cross-sectional
Evidence: low
Full summary, score breakdown and related studies →
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This study strengthens the potential of neurogranin as an AD CSF biomarker, which now needs validation in larger studies. 3 key findings →
Participants: 29
Evidence: low
Full summary, score breakdown and related studies →
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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
- 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.