In clinical samples, people with amnestic MCI are at high risk of developing Alzheimer's disease dementia, with annual rates of progression from MCI to Alzheimer's disease estimated at approximately 10% to 15% compared with the base incidence rates of Alzheimer's disease dementia of 1% to 2% per year. 5 key findings →
Design: cohort study
Participants: 33
Evidence: moderate
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An accurate blood test for Alzheimer's disease that is sensitive to preclinical proteinopathy and cognitive decline has clear implications for early detection and secondary prevention. 2 key findings →
Design: cohort study
Participants: 165
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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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
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Plasma p-tau217 showed the strongest individual association with Aβ PET status (area under the curve [AUC], 0.85). 5 key findings →
Design: cohort study
Participants: 1,407
Evidence: moderate
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Combining plasma p-tau with Aβ42 or the Aβ42/40 ratio reduced the intermediate zone. 5 key findings →
Design: cross-sectional
Participants: 326
Evidence: moderate
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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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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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70/100
✓ Peer-reviewed
alzhub usefulness score 70 out of 100.
·
JAMA network open
·
2022-04-01
These findings suggest that this blood biomarker test could allow for distinguishing individuals with brain amyloid-positive PET findings from individuals with amyloid-negative PET findings and serve as an aid for Alzheimer disease diagnosis. 4 key findings →
Design: cohort study
Participants: 249
Evidence: moderate
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81 participants with probable Alzheimer's disease and 69 healthy controls were assessed. 1 key finding →
Design: clinical trial
Participants: 81
Evidence: high
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70/100
✓ Peer-reviewed
alzhub usefulness score 70 out of 100.
·
Neurology
·
2017-10-18
The highly consistent regional hierarchy of PET-evidenced amyloid deposition across participants resembles neuropathologic observations and suggests a predictable regional sequence that may be used to stage an individual's progress of amyloid pathology in vivo. 2 key findings →
Design: cross-sectional
Participants: 667
Evidence: moderate
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Therefore, we conducted a longitudinal study to examine whether PM2.5 affects the episodic memory decline, and also explored the potential mediating role of increased neuroanatomic risk of Alzheimer's disease associated with exposure. 5 key findings →
Design: longitudinal study
Participants: 998
Evidence: moderate
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70/100
✓ Peer-reviewed
alzhub usefulness score 70 out of 100.
·
JAMA Neurology
·
2025-06-09
Of 4467 participants who underwent 9208 longitudinal cognitive sessions, 2698 (60.4%) were female, and the mean age (SD) was 74.3 (9.2) years; 3213 were cognitively unimpaired, 972 had mild cognitive impairment, and 282 had AD dementia. 2 key findings →
Design: cohort study
Participants: 4,467
Evidence: moderate
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Plasma amyloid-β peptide concentration has recently been shown to have high accuracy to predict amyloid-β plaque burden in the brain. 2 key findings →
Design: longitudinal study
Participants: 15
Evidence: moderate
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Understanding the exact pathophysiological mechanisms underlying the involvement of triggering receptor expressed on myeloid cells 2 (TREM2) related microglia activation is crucial for the development of clinical trials targeting microglia activation at different stages of Alzheimer's disease (AD). 5 key findings →
Design: longitudinal study
Participants: 1,001
Evidence: moderate
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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
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Original source
This expert workgroup review summarizes what is known about ARIA, the brain-swelling (ARIA-E) and micro-bleeding (ARIA-H) side effect seen with anti-amyloid drugs. 3 key findings →
Design: systematic-review
Evidence: high
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Original source
69/100
✓ Peer-reviewed
alzhub usefulness score 69 out of 100.
·
JAMA neurology
·
2020-07-01
This study's findings suggest that PET imaging with [18F]flortaucipir could be used to identify the density and distribution of AD-type tau pathology and the presence of high levels of AD neuropathological change, supporting a neuropathological diagnosis of AD. 4 key findings →
Participants: 64
Evidence: moderate
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69/100
✓ Peer-reviewed
alzhub usefulness score 69 out of 100.
·
Neurology
·
2016-07-01
In this community-based cohort without dementia, florbetapir uptake is associated with older age and APOE genotype. 5 key findings →
Design: longitudinal study
Participants: 329
Evidence: moderate
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ADNI has demonstrated the feasibility and utility of multicenter PET studies and is helping to clarify the role of biomarkers in the study of aging and dementia. 3 key findings →
Design: longitudinal study
Participants: 100
Evidence: moderate
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69/100
✓ Peer-reviewed
alzhub usefulness score 69 out of 100.
·
PloS one
·
2015-08-07
11 studies were identified, including 380 patients with AD, 68 with MCI and 293 healthy controls (HC). 4 key findings →
Design: meta-analysis
Participants: 380
Evidence: high
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69/100
✓ Peer-reviewed
alzhub usefulness score 69 out of 100.
·
Neurology
·
2022-08-29
The PubMed and Embase databases were searched for clinical trials of anti-Aβ immunotherapy published on or before January 12, 2022. 4 key findings →
Design: clinical trial
Participants: 9,429
Evidence: high
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The Alzheimer's Disease Neuroimaging Initiative (ADNI) is an ongoing, longitudinal, multicenter study designed to develop clinical, imaging, genetic, and biochemical biomarkers for the early detection and tracking of Alzheimer's disease (AD). 4 key findings →
Design: longitudinal study
Participants: 400
Evidence: moderate
Full summary, score breakdown and related studies →
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¹⁸F-FDFG uptake by brain tissue as measured by positron emission tomography (PET) is a well-established method for assessment of brain function in people with dementia. 4 key findings →
Design: meta-analysis
Participants: 14
Evidence: high
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.