67/100
✓ Peer-reviewed
alzhub usefulness score 67 out of 100.
·
JAMA neurology
·
2016-01-01
Cerebrospinal fluid NFL concentration (median [interquartile range]) was higher in the AD dementia group (1479 [1134-1842] pg/mL), stable MCI group (no progression to AD during follow-up; 1182 [923-1687] pg/mL), and progressive MCI group (MCI with progression to AD dementia during follow-up; 1336 [1061-1693] pg/mL) compared with control participants (1047 [809-1265] pg/mL) (P Conclusions and relevance Cerebrospinal fluid NFL concentration is increased by the early clinical stage of AD and is associated with cognitive deterioration and structural brain changes over time. 2 key findings →
Design: longitudinal study
Participants: 95
Evidence: moderate
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Plasma Aβ42/Aβ40${{\rm A}\beta }_{42}/{{\rm A}\beta }_{40}$ may begin declining decades prior to brain amyloid accumulation, whereas p-tau ratios, GFAP, and NfL increase closer in time. 1 key finding →
Design: longitudinal study
Participants: 199
Evidence: moderate
Full summary, score breakdown and related studies →
Original source
Cerebrospinal fluid (CSF) tau (total tau, T-tau), neurofilament light (NFL), and neurogranin (Ng) are potential biomarkers for neurodegeneration in Alzheimer's disease (AD). 3 key findings →
Design: longitudinal study
Participants: 93
Evidence: moderate
Full summary, score breakdown and related studies →
Original source
We found low intra-individual variability, robust to various factors, appropriate to capture individual changes in AD BBMs, while moderate inter-individual variability may give rise to caution in diagnostic contexts. 2 key findings →
Design: longitudinal study
Participants: 27
Evidence: moderate
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66/100
✓ Peer-reviewed
alzhub usefulness score 66 out of 100.
·
JAMA neurology
·
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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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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66/100
✓ Peer-reviewed
alzhub usefulness score 66 out of 100.
·
PLoS medicine
·
2020-08-20
The ε4 allele of apolipoprotein E (APOE) gene and increasing age are two of the most important known risk factors for developing Alzheimer disease (AD). 4 key findings →
Design: cohort study
Participants: 1,593
Evidence: moderate
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66/100
✓ Peer-reviewed
alzhub usefulness score 66 out of 100.
·
Drugs
·
2024-06-20
The enrolled population of 84 subjects (31 homozygotes and 53 heterozygotes) was 52% females, mean age 69 years, MMSE 25.7 [70% mild cognitive impairment (MCI), 30% mild AD] with 55% on cholinesterase inhibitors. 5 key findings →
Design: clinical trial
Participants: 80
Evidence: low
Full summary, score breakdown and related studies →
Original source
Risk stratification for PET Aβ+ based on a plasma p-tau217 assay demonstrated potential diagnostic and prognostic utility in an Asian cohort with concomitant CeVD. 4 key findings →
Participants: 142
Evidence: moderate
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Niemann-Pick disease type C and Alzheimer's disease are distinct neurodegenerative disorders that share the presence of neurofibrillary tangle pathology. 4 key findings →
Design: cross-sectional
Participants: 60
Evidence: moderate
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65/100
✓ Peer-reviewed
alzhub usefulness score 65 out of 100.
·
JAMA neurology
·
2021-09-01
In this largely presymptomatic population, these results suggest subtle differences across plasma p-tau species and platforms for the prediction of amyloid and tau PET and magnetic resonance imaging measures of cerebrovascular and Alzheimer-related pathology. 5 key findings →
Participants: 1,329
Evidence: low
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65/100
✓ Peer-reviewed
alzhub usefulness score 65 out of 100.
·
Neurology
·
2024-12-26
This study examined whether levels of blood biomarkers of amyloid (Aβ 42 /Aβ 40 ratio), tau (p-tau 181 ), neurodegeneration (NfL), and glial activation and neuroinflammation (glial fibrillary acidic protein [GFAP], YKL40, soluble triggering receptor expressed on myeloid cells 2 [sTREM2]) collected when participants were cognitively normal are associated with the time to onset of MCI. 5 key findings →
Design: longitudinal study
Participants: 271
Evidence: moderate
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65/100
✓ Peer-reviewed
alzhub usefulness score 65 out of 100.
·
Neurology
·
2023-07-27
Choroid plexus (ChP) is emerging as a key brain structure in the pathophysiology of neurodegenerative disorders. 4 key findings →
Design: longitudinal study
Participants: 135
Evidence: moderate
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64/100
✓ Peer-reviewed
alzhub usefulness score 64 out of 100.
·
Neurology
·
2016-07-01
Biomarkers have become an essential component of Alzheimer disease (AD) research and because of the pervasiveness of AD pathology in the elderly, the same biomarkers are used in cognitive aging research. 1 key finding →
Evidence: low
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We envision that defining AD as a biological construct will enable a more accurate characterization and understanding of the sequence of events that lead to cognitive impairment that is associated with AD, as well as the multifactorial etiology of dementia. 1 key finding →
Evidence: low
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Although the prevalence of dementia continues to increase worldwide, incidence in the western world might have decreased as a result of better vascular care and improved brain health. 2 key findings →
Evidence: low
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64/100
✓ Peer-reviewed
alzhub usefulness score 64 out of 100.
·
JAMA neurology
·
2014-04-01
Identifying a clinical distinction between the invariably lethal prion disease Creutzfeldt-Jakob disease (CJD) and nonprion rapidly progressive dementias is important and sometimes difficult; thus, reliable tools for diagnosis are in great demand. 4 key findings →
Design: cohort study
Participants: 30
Evidence: moderate
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Relative to controls, greater Alzheimer's disease pathology (lower amyloid-β 42 /amyloid-β 40 , higher phosphorylated-tau-181) and synaptic degeneration (neurogranin) biomarker concentrations were associated with more adverse white matter metrics (e.g. lower neurite density, higher mean diffusivity) in patients with asthma. 4 key findings →
Design: case-control study
Evidence: moderate
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Original source
64/100
✓ Peer-reviewed
alzhub usefulness score 64 out of 100.
·
JAMA neurology
·
2015-10-01
Among the 128 study participants, the 104 patients with early PD had a different CSF pattern compared with the 13 patients with progressive supranuclear palsy (baseline area under the receiver operating characteristic curve, 0.87; P < .0001) and the 30 control participants (baseline area under the receiver operating characteristic curve, 0.69; P = .0021). 2 key findings →
Design: cohort study
Participants: 104
Evidence: moderate
Full summary, score breakdown and related studies →
Original source
Perioperative changes in plasma amyloid do not appear to be associated with postoperative delirium. 5 key findings →
Design: cohort study
Participants: 100
Evidence: moderate
Full summary, score breakdown and related studies →
Original source
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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63/100
✓ Peer-reviewed
alzhub usefulness score 63 out of 100.
·
Neurology
·
2023-05-03
Pericyte damage, reflected by CSF PDGFRβ, may be involved in age-related BBB disruption together with neuroinflammation, but is not related to Alzheimer-related pathologic changes. 2 key findings →
Participants: 408
Evidence: moderate
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62/100
✓ Peer-reviewed
alzhub usefulness score 62 out of 100.
·
JAMA network open
·
2025-05-01
Lobar CMB counts and the presence of CAA were associated with downstream AD plasma biomarkers, including p-tau217 (β = 0.12 [95% CI, 0.05-0.18] and 0.29 [95% CI, 0.12-0.47], respectively), GFAP (β = 0.07 [95% CI, 0.03-0.12] and 0.20 [95% CI, 0.09-0.31], respectively), and NfL (β = 0.07 [95% CI, 0.03-0.11] and 0.16 [95% CI, 0.06-0.25], respectively) with and without the mediation of Aβ uptake on PET (indirect effect: lobar CMBs-p-tau217, 59.8% [β = 0.07 (95% CI, 0.03-0.11)]; lobar CMBs-GFAP, 49.3% [β = 0.04 (95% CI, 0.01-0.06)]; lobar CMBs-NfL, 20.9% [β = 0.01 (95% CI, 0.01-0.03)]; CAA-p-tau217, 50.9% [β = 0.15 (95% CI, 0.06-0.24)]; CAA-GFAP, 39.2% [β = 0.08 (95% CI, 0.03-0.13)]; CAA-NfL, 19.2% [β = 0.03 (95% CI, 0.01-0.05)]). 4 key findings →
Design: cohort study
Participants: 1,708
Evidence: moderate
Full summary, score breakdown and related studies →
Original source
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This study questions the effect of statins on the processing of amyloid precursor protein in humans. 4 key findings →
Evidence: high
Full summary, score breakdown and related studies →
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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
Full summary, score breakdown and related studies →
Original source
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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 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.