We found a sequence to pathological changes, with rates of Aβ deposition in mutation carriers being significantly different from those in non-carriers first (across regions that showed a significant difference, at a mean of 18·9 years [SD 3·3] before expected onset), followed by hypometabolism (14·1 years [5·1] before expected onset), and lastly structural decline (4·7 years [4·2] before expected onset). 2 key findings →
Design: longitudinal study
Participants: 346
Evidence: moderate
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76/100
✓ Peer-reviewed
alzhub usefulness score 76 out of 100.
·
JAMA
·
2025-06-16
Among the 6514 participants (mean age, 69.5 years; 50.5% female), median follow-up time ranged from 1.5 to 4.0 years. 5 key findings →
Design: longitudinal study
Participants: 6,514
Evidence: moderate
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Although studies in animal models suggest that TREM2 is protective against Alzheimer's pathology, its effect on tau pathology and its potential beneficial role in people with Alzheimer's disease is still unclear. 4 key findings →
Design: longitudinal study
Participants: 155
Evidence: moderate
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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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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
·
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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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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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.
·
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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CSF Aβ42 levels are tightly coupled with cortical amyloid load in the earliest stages of preclinical AD, and begin to decrease dramatically prior to the point when an abnormal threshold of cortical accumulation is detected with amyloid imaging. 1 key finding →
Design: longitudinal study
Participants: 164
Evidence: moderate
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64/100
✓ Peer-reviewed
alzhub usefulness score 64 out of 100.
·
JAMA neurology
·
2016-10-01
Among the 174 participants (81 men [46.6%]; 93 women [53.4%]; mean [SD] age, 65.7 [8.9] years), a proportion (14%-17%) of individuals with neurodegeneration alone (SNAP) later demonstrated Aβ+. 1 key finding →
Design: cohort study
Participants: 174
Evidence: moderate
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Autosomal-dominant AD is associated with increased WMH well before expected symptom onset. 4 key findings →
Participants: 299
Evidence: low
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62/100
✓ Peer-reviewed
alzhub usefulness score 62 out of 100.
·
Neurology
·
2011-04-27
Changes in functional connectivity in DLB indicate patterns of activation that are distinct from those seen in AD and may improve discrimination of DLB from AD and cognitively normal individuals. 3 key findings →
Design: longitudinal study
Participants: 88
Evidence: moderate
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61/100
✓ Peer-reviewed
alzhub usefulness score 61 out of 100.
·
JAMA neurology
·
2018-05-01
Preclinical AD is associated with rest-activity rhythm fragmentation, independent of age or sex. 5 key findings →
Design: cross-sectional
Participants: 205
Evidence: moderate
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Preclinical AD as detected by PET PiB is not benign, as it is associated with progression to symptomatic AD. 4 key findings →
Design: cohort study
Evidence: moderate
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Clinicopathological evidence suggests that the pathology of Alzheimer's disease (AD) begins many years before the appearance of cognitive symptoms. 3 key findings →
Design: cross-sectional
Evidence: moderate
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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.
·
JAMA neurology
·
2014-09-01
Resting-state functional connectivity magnetic resonance imaging changes with progressing AD severity are similar between ADAD and LOAD. 2 key findings →
Design: cross-sectional
Participants: 79
Evidence: moderate
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Symptomatic mutation carriers also demonstrated elevated tau PET binding in the basal ganglia, consistent with prior work with amyloid-β. 2 key findings →
Design: cross-sectional
Evidence: low
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59/100
✓ Peer-reviewed
alzhub usefulness score 59 out of 100.
·
Neurology
·
2013-09-18
Atrophy in FAD is observed early, both in areas commonly associated with sporadic Alzheimer disease and also in the putamen and thalamus, 2 regions associated with early amyloid deposition in FAD mutation carriers. 4 key findings →
Design: cross-sectional
Participants: 192
Evidence: low
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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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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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58/100
✓ Peer-reviewed
alzhub usefulness score 58 out of 100.
·
Cerebral Cortex
·
2008-07-16
Alzheimer's disease (AD) is associated with neurodegeneration in vulnerable limbic and heteromodal regions of the cerebral cortex, detectable in vivo using magnetic resonance imaging.
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These findings suggest that CSF VILIP-1 and VILIP-1/Aβ42 offer diagnostic utility for early AD, and can predict future cognitive impairment in cognitively normal individuals similarly to tau and tau/Aβ42, respectively. 3 key findings →
Participants: 211
Evidence: moderate
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Alzheimer's disease (AD) and antecedent factors associated with AD were explored using amyloid imaging and unbiased measures of longitudinal atrophy in combination with reanalysis of previous metabolic and functional 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 28,580 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.