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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79/100
✓ Peer-reviewed
alzhub usefulness score 79 out of 100.
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JAMA
·
2024-10-15
Plasma biomarkers of AD neuropathology, neuronal injury, and astrogliosis increase with age and are associated with known dementia risk factors. 5 key findings →
Design: cohort
Participants: 1,525
Evidence: high
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79/100
✓ Peer-reviewed
alzhub usefulness score 79 out of 100.
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JAMA neurology
·
2023-04-01
Among 171 Aβ-positive CU participants included in the main analyses, 119 (mean [SD] age, 73.0 [5.4] years; 60.5% female) were from the BioFINDER-1 study, and 52 (mean [SD] age, 64.4 [4.6] years; 65.4% female) were from the WRAP study. 2 key findings →
Design: cohort study
Participants: 564
Evidence: moderate
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77/100
✓ Peer-reviewed
alzhub usefulness score 77 out of 100.
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JAMA Neurology
·
2024-01-01
Of a total 912 participants, there were 499 males (54.7%) and 413 females (45.3%), and the mean (SD) age was 71.1 (8.49) years. 5 key findings →
Design: cohort
Participants: 912
Evidence: high
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77/100
✓ Peer-reviewed
alzhub usefulness score 77 out of 100.
·
Nature medicine
·
2025-03-31
Rates of cognitive decline in Alzheimer's disease (AD) are extremely heterogeneous. 1 key finding →
Design: case-control study
Participants: 3,397
Evidence: moderate
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76/100
✓ Peer-reviewed
alzhub usefulness score 76 out of 100.
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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.
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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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75/100
✓ Peer-reviewed
alzhub usefulness score 75 out of 100.
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JAMA neurology
·
2021-12-01
This study suggests that plasma GFAP is a sensitive biomarker for detecting and tracking reactive astrogliosis and Aβ pathology even among individuals in the early stages of AD. 5 key findings →
Design: cross-sectional
Participants: 300
Evidence: moderate
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Cerebrospinal fluid (CSF) p-tau181 (tau phosphorylated at threonine 181) is an established biomarker of Alzheimer's disease (AD), reflecting abnormal tau metabolism in the brain. 3 key findings →
Design: longitudinal study
Participants: 194
Evidence: moderate
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74/100
✓ Peer-reviewed
alzhub usefulness score 74 out of 100.
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Nature medicine
·
2019-01-21
Neurofilament light chain (NfL) is a promising fluid biomarker of disease progression for various cerebral proteopathies. 2 key findings →
Design: cross-sectional
Participants: 187
Evidence: moderate
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74/100
✓ Peer-reviewed
alzhub usefulness score 74 out of 100.
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Nature medicine
·
2024-02-21
With the emergence of Alzheimer's disease (AD) disease-modifying therapies, identifying patients who could benefit from these treatments becomes critical. 1 key finding →
Participants: 1,422
Evidence: moderate
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We performed a meta-analysis to examine the aggregate levels of serum BDNF in patients with AD and individuals with MCI, in comparison with healthy controls. 4 key findings →
Design: meta-analysis
Participants: 2,067
Evidence: high
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73/100
✓ Peer-reviewed
alzhub usefulness score 73 out of 100.
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JAMA network open
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2025-02-03
The mean (SD) baseline age of 758 participants was 61.5 (6.1) years, and 424 participants [55.9%] were female. 4 key findings →
Design: cohort study
Participants: 758
Evidence: high
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Amyloid-beta 42 (Aβ42) and phosphorylated tau (pTau) levels in cerebrospinal fluid (CSF) reflect core features of the pathogenesis of Alzheimer's disease (AD) more directly than clinical diagnosis. 2 key findings →
Participants: 8,074
Evidence: low
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73/100
✓ Peer-reviewed
alzhub usefulness score 73 out of 100.
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Neurology
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2018-07-27
Neuroinflammation and cerebrovascular dysfunction are early events occurring already at presymptomatic stages of AD and contribute to disease progression. 5 key findings →
Design: longitudinal study
Participants: 508
Evidence: moderate
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73/100
✓ Peer-reviewed
alzhub usefulness score 73 out of 100.
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Neuron
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2025-03-14
Changes in β-amyloid (Aβ) and hyperphosphorylated tau (T) in brain and cerebrospinal fluid (CSF) precede Alzheimer's disease (AD) symptoms, making the CSF proteome a potential avenue to understand disease pathophysiology and facilitate reliable diagnostics and therapies. 5 key findings →
Design: meta-analysis
Evidence: high
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72/100
✓ Peer-reviewed
alzhub usefulness score 72 out of 100.
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JAMA
·
2024-10-01
The mean age was 74.2 years (SD, 8.3 years), 48% were women, 23% had subjective cognitive decline, 44% had mild cognitive impairment, and 33% had dementia. 2 key findings →
Participants: 307
Evidence: moderate
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72/100
✓ Peer-reviewed
alzhub usefulness score 72 out of 100.
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Neurology
·
2015-09-09
The best CSF measures for identifying MCI-AD were Aβ42/total tau (t-tau) and Aβ42/hyperphosphorylated tau (p-tau) (area under the curve [AUC] 0.93-0.94). 3 key findings →
Design: longitudinal study
Participants: 122
Evidence: moderate
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72/100
✓ Peer-reviewed
alzhub usefulness score 72 out of 100.
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Neurology
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2020-01-08
In response to sleep loss (+17.2%), compared with normal sleep (+1.8%), the evening to morning ratio was increased for t-tau ( p = 0.035). 4 key findings →
Evidence: high
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72/100
✓ Peer-reviewed
alzhub usefulness score 72 out of 100.
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JAMA neurology
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2023-04-01
In this case-control study, blood biomarkers indicative of AD pathology demonstrated different dynamics of change after cardiac arrest. 5 key findings →
Design: case-control study
Participants: 80
Evidence: high
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72/100
✓ Peer-reviewed
alzhub usefulness score 72 out of 100.
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Neurology
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2024-07-10
We demonstrated significant elevations in blood GFAP and YKL-40 levels in patients on the AD continuum compared with CU individuals. 5 key findings →
Design: systematic review
Participants: 3,366
Evidence: high
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Antioxidants did not influence CSF biomarkers related to amyloid or tau pathology. 1 key finding →
Evidence: high
Full summary, score breakdown and related studies →
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Cerebral accumulation of amyloid-β is thought to be the starting mechanism in Alzheimer's disease. 4 key findings →
Design: longitudinal study
Participants: 437
Evidence: moderate
Full summary, score breakdown and related studies →
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Neuroinflammatory biomarkers are associated with AD progression. 5 key findings →
Design: meta-analysis
Evidence: high
Full summary, score breakdown and related studies →
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71/100
✓ Peer-reviewed
alzhub usefulness score 71 out of 100.
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Brain
·
2024-05-03
The main findings demonstrated an association between serum GFAP level and post-mortem tau pathology (β = 12.85; P < 0.001) that was independent of amyloid deposits (β = 13.23; P = 0.02). 5 key findings →
Design: cohort
Participants: 139
Evidence: moderate
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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 27,380 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.