Epidemiological studies have identified a robust association between type II diabetes mellitus and Alzheimer disease (AD), and neurobiological studies have suggested the presence of central nervous system insulin resistance in individuals with AD. 3 key findings →
Evidence: high
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69/100
✓ Peer-reviewed
alzhub usefulness score 69 out of 100.
·
Nature aging
·
2024-03-21
Biological staging of individuals with Alzheimer's disease (AD) may improve diagnostic and prognostic workup of dementia in clinical practice and the design of clinical trials. 4 key findings →
Design: longitudinal study
Participants: 426
Evidence: moderate
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Amyloid chronicity provides unique information about cognitive decline and neurofibrillary tangle development and may be useful to investigate preclinical Alzheimer's disease. 2 key findings →
Design: longitudinal study
Participants: 257
Evidence: moderate
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We found little evidence to support wide-ranging effects of statins on health outcomes beyond their established beneficial effect on vascular disease. 4 key findings →
Design: cohort study
Participants: 129,288
Evidence: high
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Primary include several amyloid PET measurements (Centiloid, SUVr, BPND , R1 ), and secondary are their changes from baseline, relationship to other amyloid markers (cerebrospinal fluid and visual assessment), and predictive value of AD-related decline. 2 key findings →
Design: cohort study
Participants: 2,000
Evidence: moderate
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Twelve articles-published between the 2007 and 2017-have been included in this systematic review after a quantitative and qualitative selection. 4 key findings →
Design: systematic review
Evidence: high
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68/100
✓ Peer-reviewed
alzhub usefulness score 68 out of 100.
·
JAMA neurology
·
2020-08-01
In this study, elevated [18F]RO948 SUVRs were most often seen among Aβ-positive cases, which suggests that [18F]RO948 has high specificity for AD-type tau and highlights its potential as a diagnostic marker in the differential diagnosis of AD. 4 key findings →
Design: cross-sectional
Participants: 257
Evidence: low
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68/100
✓ Peer-reviewed
alzhub usefulness score 68 out of 100.
·
Neurology
·
2017-11-01
Our prospective findings provide evidence for what may be an early contributory role of systemic inflammation in neurodegeneration and cognitive aging. 3 key findings →
Design: cohort study
Participants: 1,633
Evidence: moderate
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68/100
✓ Peer-reviewed
alzhub usefulness score 68 out of 100.
·
JAMA network open
·
2019-05-03
In this study, lower AD signature region volumes, brain microhemorrhages, higher WMH volumes, and infarcts were risk factors associated with dementia in older community-based residents. 4 key findings →
Design: cohort study
Participants: 1,553
Evidence: moderate
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68/100
✓ Peer-reviewed
alzhub usefulness score 68 out of 100.
·
Brain
·
2016-03-08
Voxel-wise contrasts against controls (at P < 0.05 family-wise error corrected) showed that (18)F-AV1451 and (18)F-FDG patterns in patients with posterior cortical atrophy ('visual variant of Alzheimer's disease', n = 7) specifically targeted the clinically affected posterior brain regions, while (11)C-PiB bound diffusely throughout the neocortex. 5 key findings →
Participants: 20
Evidence: low
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53/310 (17.1%) subjects were classified as Focal-FMM. 5 key findings →
Design: longitudinal study
Participants: 310
Evidence: moderate
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This study analyzed 871 eyes from 439 participants (230 APOE ε4 noncarriers and 209 carriers). 5 key findings →
Design: longitudinal study
Participants: 58
Evidence: moderate
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The very mildest symptomatic stage of AD exhibits the same CSF biomarker phenotype as more advanced AD. 1 key finding →
Design: longitudinal study
Participants: 139
Evidence: moderate
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67/100
✓ Peer-reviewed
alzhub usefulness score 67 out of 100.
·
Neurology
·
2019-01-09
Our findings suggest that tau PET is more sensitive than Aβ PET and measures of cortical thickness for detecting early cognitive changes in preclinical AD. 2 key findings →
Design: cross-sectional
Participants: 106
Evidence: low
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67/100
✓ Peer-reviewed
alzhub usefulness score 67 out of 100.
·
Neurology
·
2008-12-24
Thinning in specific cortical areas known to be affected by Alzheimer disease (AD) is detectable in individuals with questionable AD dementia (QAD) and predicts conversion to mild AD dementia. 3 key findings →
Design: longitudinal study
Participants: 49
Evidence: moderate
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The findings suggest that midlife HI is a risk factor for temporal lobe volume loss. 5 key findings →
Design: cohort study
Participants: 194
Evidence: moderate
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67/100
✓ Peer-reviewed
alzhub usefulness score 67 out of 100.
·
PLoS medicine
·
2021-05-27
We tested whether dysregulation of cholesterol catabolism, through its conversion to primary bile acids (BAs), was associated with dementia pathogenesis. 5 key findings →
Design: cohort study
Participants: 141
Evidence: moderate
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67/100
✓ Peer-reviewed
alzhub usefulness score 67 out of 100.
·
JAMA neurology
·
2023-12-01
Data from 3960 MRI sessions among 1141 participants were included: 252 pathogenic variant carriers from DIAN (mean [SD] age, 38.4 [11.2] years; 137 [54%] female), 571 older adults from ADNI (mean [SD] age, 72.8 [7.3] years; 274 [48%] female), and 318 older adults from HABS (mean [SD] age, 72.4 [7.6] years; 194 [61%] female). 3 key findings →
Design: cohort study
Participants: 1,141
Evidence: moderate
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PSMD is a new, fully automated, and robust imaging marker for SVD. 3 key findings →
Design: longitudinal study
Participants: 113
Evidence: moderate
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67/100
✓ Peer-reviewed
alzhub usefulness score 67 out of 100.
·
Brain
·
2020-04-29
Principal component analysis identified patterns of variation in baseline and longitudinal measures of tau uptake and volume that were significantly different across phenotypes. 2 key findings →
Design: longitudinal study
Participants: 57
Evidence: moderate
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66/100
✓ Peer-reviewed
alzhub usefulness score 66 out of 100.
·
Neurology
·
2006-08-01
Longitudinal studies will be required to determine the association of elevated [(11)C]PIB binding and risk of developing dementia of the Alzheimer type. 2 key findings →
Design: longitudinal study
Evidence: moderate
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66/100
✓ Peer-reviewed
alzhub usefulness score 66 out of 100.
·
Diabetes care
·
2013-08-12
Neurodegeneration rather than cerebrovascular lesions may play a key role in T2DM-related cognitive impairment. 2 key findings →
Design: cross-sectional
Participants: 350
Evidence: low
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66/100
✓ Peer-reviewed
alzhub usefulness score 66 out of 100.
·
Neurology
·
2005-08-01
Hippocampal volume was the primary determinant of memory decline, whereas executive function (EXEC) decline was related to multiple brain components. 5 key findings →
Design: longitudinal study
Participants: 103
Evidence: moderate
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66/100
✓ Peer-reviewed
alzhub usefulness score 66 out of 100.
·
JAMA neurology
·
2022-10-01
Among 580 participants (PREVENT-AD, 128; HABS, 153; AIBL, 48; Knight ADRC, 251), mean (SD) age ranged from 67 (5) to 76 (6) years across cohorts, with between 55% (137/251) and 74% (95/128) female participants. 2 key findings →
Design: cohort study
Participants: 580
Evidence: moderate
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66/100
✓ Peer-reviewed
alzhub usefulness score 66 out of 100.
·
Neurology
·
2021-04-14
In this longitudinal study of cognitively unimpaired adults, living in the most highly disadvantaged neighborhoods was associated with accelerated degeneration in Alzheimer signature regions and cognitive decline. 5 key findings →
Design: longitudinal study
Participants: 19
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.