60/100
✓ Peer-reviewed
alzhub usefulness score 60 out of 100.
·
Neurology
·
2009-10-01
Different biomarkers for Alzheimer disease provide different information from one another that is likely to be complementary. 1 key finding →
Participants: 34
Evidence: low
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60/100
✓ Peer-reviewed
alzhub usefulness score 60 out of 100.
·
Neurology
·
2012-09-12
Increased WMHs are associated with aging, decreased glucose metabolism, and decline in executive function but do not affect AD-specific pathologic progression, suggesting that the vascular contribution to dementia is probably additive although not necessarily independent of the amyloid pathway. 5 key findings →
Design: longitudinal study
Evidence: moderate
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60/100
✓ Peer-reviewed
alzhub usefulness score 60 out of 100.
·
NeuroImage
·
2009-01-21
In mostly small single-center studies, Alzheimer's disease (AD) is associated with characteristic and progressive reductions in fluorodeoxyglucose positron emission tomography (PET) measurements of the regional cerebral metabolic rate for glucose (CMRgl). 4 key findings →
Design: longitudinal study
Evidence: moderate
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Using data from the Alzheimer's Disease Neuroimaging Initiative (ADNI) population, we examined (1) cross-sectional relationships between amyloid deposition, hypometabolism, and cognition, and (2) associations between amyloid and hypometabolism measurements and longitudinal cognitive measurements. 4 key findings →
Design: cross-sectional
Evidence: moderate
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A biological research framework to define Alzheimer' disease with dichotomized biomarker measurement was proposed by National Institute on Aging-Alzheimer's Association (NIA-AA). 3 key findings →
Design: longitudinal study
Evidence: moderate
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Cerebrospinal fluid and positron emission tomography amyloid-β were measured at baseline in 769 persons [161 healthy controls, 68 subjective memory complaints, 419 mild cognitive impairment and 121 Alzheimer's disease dementia, mean age 72 years (standard deviation 7 years), 47% females] and used to predict diagnosis, APOE ε4 carriage status, cerebral blood flow, cerebrospinal fluid total-tau and phosphorylated-tau levels (cross-sectionally); and hippocampal volume, fluorodeoxyglucose positron emission tomography results and Alzheimer's Disease Assessment Scale-cognitive subscale scores (longitudinally). 2 key findings →
Participants: 769
Evidence: low
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The mechanisms underpinning concussion, traumatic brain injury, and chronic traumatic encephalopathy, and the relationships between these disorders, are poorly understood. 4 key findings →
Evidence: low
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58/100
✓ Peer-reviewed
alzhub usefulness score 58 out of 100.
·
Neurology
·
2026-02-02
's ≥ 0.75). Both markers identified Braak stage V-VI levels with similarly high performance (entorhinal SUVR, area under the curve [AUC] = 0.92 [95% CI 0.91-0.93]; temporal meta-ROI SUVR, AUC = 0.91 [95% CI 0.90-0.92]; plasma p-tau217, AUC = 0.90 [95% CI 0.89-0.91]), but PET outperformed plasma p-tau217 in identifying high/intermediate ADNCs (entorhinal ROI, AUC = 0.94 [95% CI 0.94-0.95]; temporal meta-ROI AUC = 0.94 [95% CI 0.94-0.95]; plasma p-tau217, AUC = 0.89 [95% CI 0.88-0.90]). 2 key findings →
Participants: 56
Evidence: moderate
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58/100
✓ Peer-reviewed
alzhub usefulness score 58 out of 100.
·
JAMA Neurology
·
2026-06-29
In 272 participants, mean (SD) age was 70 (4.5) years, 270 were male (99.3%), and 83 (30.5%) were amyloid-PET positive. 5 key findings →
Design: cohort study
Participants: 272
Evidence: moderate
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58/100
✓ Peer-reviewed
alzhub usefulness score 58 out of 100.
·
BMJ Open
·
2025-08-01
Fit of the models to the data was adequate for general cognitive performance (root mean squared error of approximation (RMSEA)=0.03; comparative fit index (CFI)=0.94; standardised root mean residual (SRMR)=0.05), language (RMSEA=0.02; CFI=0.95; SRMR=0.05) and good for memory (RMSEA=0.05; CFI=0.99; SRMR=0.02) and executive functioning (RMSEA=0.03; CFI=0.98; SRMR=0.03). 5 key findings →
Design: cohort study
Participants: 5,878
Evidence: moderate
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Although amyloid imaging with PiB-PET ([C-11]Pittsburgh Compound-B positron emission tomography), and now with F-18-labeled tracers, has produced remarkably consistent qualitative findings across a large number of centers, there has been considerable variability in the exact numbers reported as quantitative outcome measures of tracer retention. 4 key findings →
Evidence: low
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57/100
✓ Peer-reviewed
alzhub usefulness score 57 out of 100.
·
Neurology
·
2021-01-06
Lowering brain Aβ must be accomplished early in the evolution of AD. 4 key findings →
Participants: 475
Evidence: low
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18 F-flortaucipir uptake was elevated in PSP versus controls and PD patients in a pattern consistent with the expected distribution of tau pathology. 3 key findings →
Participants: 33
Evidence: low
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Based on previous studies, a preclinical classification for Alzheimer's disease (AD) has been proposed. 4 key findings →
Design: cross-sectional
Participants: 160
Evidence: moderate
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Magnetic resonance (MR) imaging is used widely for assessment of patients with cognitive impairment, but the pathological correlates are unclear, especially when multiple pathologies are present. 4 key findings →
Participants: 93
Evidence: moderate
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Patients with Alzheimer's disease have reduced cerebral blood flow measured by arterial spin labelling magnetic resonance imaging, but it is unclear how this is related to amyloid-β pathology. 4 key findings →
Participants: 51
Evidence: low
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Among the participants, 377 (93.5%) reported subjective memory complaints. 5 key findings →
Design: longitudinal study
Participants: 403
Evidence: moderate
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The extent to which the pathophysiology of autosomal dominant Alzheimer's disease corresponds to the pathophysiology of 'sporadic' late onset Alzheimer's disease is unknown, thus limiting the extrapolation of study findings and clinical trial results in autosomal dominant Alzheimer's disease to late onset Alzheimer's disease. 3 key findings →
Participants: 559
Evidence: low
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56/100
✓ Peer-reviewed
alzhub usefulness score 56 out of 100.
·
NeuroImage
·
2017-06-03
The recent development of tau-specific positron emission tomography (PET) tracers enables in vivo quantification of regional tau pathology, one of the key lesions in Alzheimer's disease (AD). 2 key findings →
Evidence: low
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56/100
✓ Peer-reviewed
alzhub usefulness score 56 out of 100.
·
JAMA neurology
·
2018-02-01
These findings suggest that patterns of cortical Aβ and tau do not differ in people with PD-CN, people with PD-MCI, and healthy older adults. 5 key findings →
Design: cross-sectional
Participants: 30
Evidence: low
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56/100
✓ Peer-reviewed
alzhub usefulness score 56 out of 100.
·
NeuroImage
·
2014-10-29
Positive cerebrospinal fluid (CSF) biomarkers of tau and amyloid beta42 suggest possible active underlying Alzheimer's disease (AD) including neurometabolic dysfunction and neurodegeneration leading to eventual cognitive decline. 4 key findings →
Design: cohort study
Participants: 82
Evidence: moderate
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56/100
✓ Peer-reviewed
alzhub usefulness score 56 out of 100.
·
Neurology
·
2005-08-01
Despite advances in the clinical characterization of FTD, little is known about its rate of progression. 4 key findings →
Participants: 70
Evidence: low
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The rural setting presented unique challenges including: low literacy rates (60.1% of participants had no schooling), diverse language use (primarily Giriama and Swahili), limited infrastructure (e.g., 44.8% of households had electricity), restrictive cultural norms that influenced data collection (e.g., in-home interviews were often conducted outdoors with destructions). 5 key findings →
Design: longitudinal study
Participants: 202
Evidence: moderate
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Education, occupation, premorbid intelligence, and brain size are surrogate markers for cognitive reserve. 1 key finding →
Design: longitudinal study
Participants: 819
Evidence: moderate
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55/100
✓ Peer-reviewed
alzhub usefulness score 55 out of 100.
·
JAMA network open
·
2025-08-01
A substantial difference in the type of therapeutics researched was observed, with anti-amyloid and anti-tau RCTs being more likely to be funded by the pharmaceutical industry compared with neurotransmitter or other RCTs (anti-amyloid or anti-tau, 68 of 71 [95.8%]; neurotransmitter, 52 of 69 [77.6%]; other, 33 of 52 [63.5%]). 2 key findings →
Design: clinical trial
Participants: 203
Evidence: high
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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.