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
Full summary, score breakdown and related studies →
Original source
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Plasma pTau217R matched CSF eMTBR-tau243 and outperformed MTBR-tau243. 5 key findings →
Participants: 242
Evidence: low
Full summary, score breakdown and related studies →
Original source
73/100
✓ Peer-reviewed
alzhub usefulness score 73 out of 100.
·
PLoS medicine
·
2018-01-25
We found that distinct sphingolipid species including sphingomyelin (SM) with acyl residue sums C16:0, C18:1, and C16:1 (SM C16:0, SM C18:1, SM C16:1) and hydroxysphingomyelin with acyl residue sum C14:1 (SM (OH) C14:1) were consistently associated with severity of AD pathology at autopsy and AD progression across prodromal and preclinical stages. 5 key findings →
Design: longitudinal study
Participants: 44
Evidence: moderate
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73/100
✓ Peer-reviewed
alzhub usefulness score 73 out of 100.
·
JAMA
·
2017-06-01
Among the 445 participants (243 with normal amyloid, 202 with elevated amyloid), mean (SD) age was 74.0 (5.9) years, mean education was 16.4 (2.7) years, and 52% were women. 2 key findings →
Design: longitudinal study
Participants: 243
Evidence: moderate
Full summary, score breakdown and related studies →
Original source
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The Alzheimer's Disease Neuroimaging Initiative (ADNI) is a longitudinal multisite observational study of healthy elders, mild cognitive impairment (MCI), and Alzheimer's disease. 5 key findings →
Design: longitudinal study
Evidence: moderate
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71/100
✓ Peer-reviewed
alzhub usefulness score 71 out of 100.
·
Nature medicine
·
2021-04-29
Alzheimer's disease (AD) is characterized by the spread of tau pathology throughout the cerebral cortex. 2 key findings →
Design: longitudinal study
Participants: 1,612
Evidence: moderate
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Original source
We found that the cognitively unimpaired amyloid-β-negative individuals had significant longitudinal tau accumulation confined to the PET Braak-like stage I (3.9%) and II (2.8%) areas. 4 key findings →
Design: longitudinal study
Participants: 125
Evidence: moderate
Full summary, score breakdown and related studies →
Original source
The best-performing MRI-free approaches had high continuous and dichotomous agreement with MRI-dependent SUVRs for Aβ PET and temporal flortaucipir (R2 ≥0.95; ± agreement ≥92%) and for Alzheimer's disease-related effect sizes; agreement was slightly lower for entorhinal flortaucipir and longitudinal slopes. 2 key findings →
Design: longitudinal study
Participants: 1,290
Evidence: moderate
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Original source
There were 571 participants in the normal cognition group, 625 participants in the subjective cognitive decline group, 155 participants in the objectively defined subtle cognitive decline group, 501 participants in the mild cognitive impairment group, 471 participants in Alzheimer's disease group, and 128 participants with cognitive impairment from other known causes. 5 key findings →
Design: longitudinal study
Participants: 4,386
Evidence: moderate
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Original source
Participants with CIND displayed lower perfusion in the PCC+PCu relative to participants who were CN, but there was no statistically significant difference between the groups in amyloid burden in this region. 5 key findings →
Design: case-control study
Participants: 113
Evidence: moderate
Full summary, score breakdown and related studies →
Original source
CL was associated with syndromic (F = 4.42, p = 0.014) and etiological diagnosis (F = -12.66, p < 0.001), with Alzheimer's disease (AD) patients showing the highest amyloid burden (62.9 ± 27.5), followed by dementia with Lewy bodies (DLB) (25.3 ± 35.5) and cardiovascular disease (CVD) (16.7 ± 24.5), and finally frontotemporal lobe degeneration (FTLD) (5.0 ± 17.22, t = -12.66, p < 0.001). 4 key findings →
Design: longitudinal study
Participants: 157
Evidence: moderate
Full summary, score breakdown and related studies →
Original source
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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Original source
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
Full summary, score breakdown and related studies →
Original source
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
Full summary, score breakdown and related studies →
Original source
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53/310 (17.1%) subjects were classified as Focal-FMM. 5 key findings →
Design: longitudinal study
Participants: 310
Evidence: moderate
Full summary, score breakdown and related studies →
Original source
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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Original source
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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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Original source
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
Full summary, score breakdown and related studies →
Original source
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66/100
✓ Peer-reviewed
alzhub usefulness score 66 out of 100.
·
Neurology
·
2017-06-07
In clinically normal older adults, lower functional connectivity predicted more rapid decline in PACC scores over time, particularly when coupled with increased Aβ burden. 2 key findings →
Design: longitudinal study
Participants: 237
Evidence: moderate
Full summary, score breakdown and related studies →
Original source
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Progressive tau accumulation may be more prominent in ε4 carriers, particularly in the medial and lateral temporal cortices. 1 key finding →
Design: longitudinal study
Participants: 272
Evidence: moderate
Full summary, score breakdown and related studies →
Original source
In the Asan cohort, after adjusting for age and sex, p-tau181 (AUC = 0.854) or APOE ε4 status (AUC = 0.769) distinguished Aβ status with high accuracy. 5 key findings →
Design: cohort study
Evidence: moderate
Full summary, score breakdown and related studies →
Original source
We found that 50 of 313 (∼16%) FTP scans had high levels of skull signal. 5 key findings →
Design: longitudinal study
Participants: 152
Evidence: moderate
Full summary, score breakdown and related studies →
Original source
65/100
✓ Peer-reviewed
alzhub usefulness score 65 out of 100.
·
Neurology
·
2009-08-01
Atrophy is not uniform across regions, nor does it follow a linear trajectory. 2 key findings →
Design: longitudinal study
Participants: 472
Evidence: moderate
Full summary, score breakdown and related studies →
Original source
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65/100
✓ Peer-reviewed
alzhub usefulness score 65 out of 100.
·
Neurology
·
2019-02-22
In this in vivo study, we have demonstrated that microglial activation quantified using [ 11 C]PBR28 PET was associated with higher gray matter volume and higher hippocampal volume in patients with MCI. 4 key findings →
Design: longitudinal study
Participants: 55
Evidence: moderate
Full summary, score breakdown and related studies →
Original source
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Our main findings were: (i) FDG-PET uptake in the bilateral anterior cingulate cortex and anterior temporal pole was associated with baseline global cognition in cognitively stable 80+ (the resilience signature); (ii) established Alzheimer's disease imaging biomarkers did not predict baseline global cognition in this subset of participants; (iii) in the full MCSA 80+ and ADNI cohorts, amyloid burden and FDG-PET in the resilience signature were the stronger predictors of baseline global cognition; (iv) sex and systemic vascular health predicted FDG-PET in the resilience signature, suggesting vascular health maintenance as a potential pathway to preserve the metabolism of these areas; and (v) the resilience signature provided significant information about global longitudinal cognitive change even when considering amyloid status in both the MCSA and ADNI cohorts. 1 key finding →
Design: longitudinal study
Participants: 192
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 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.