65/100
✓ Peer-reviewed
alzhub usefulness score 65 out of 100.
·
Neurology
·
2024-12-26
This study examined whether levels of blood biomarkers of amyloid (Aβ 42 /Aβ 40 ratio), tau (p-tau 181 ), neurodegeneration (NfL), and glial activation and neuroinflammation (glial fibrillary acidic protein [GFAP], YKL40, soluble triggering receptor expressed on myeloid cells 2 [sTREM2]) collected when participants were cognitively normal are associated with the time to onset of MCI. 5 key findings →
Design: longitudinal study
Participants: 271
Evidence: moderate
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65/100
✓ Peer-reviewed
alzhub usefulness score 65 out of 100.
·
Neurology
·
2025-06-25
Greater neighborhood disadvantage was associated with elevated inflammatory and AD CSF biomarkers cross-sectionally and longitudinal increases in a nonspecific inflammatory blood biomarker. 5 key findings →
Design: longitudinal study
Participants: 334
Evidence: moderate
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65/100
✓ Peer-reviewed
alzhub usefulness score 65 out of 100.
·
Neurology
·
2020-06-25
All synaptic biomarkers tested had a good discriminatory power to distinguish patients with AD abnormal CSF from those with non-AD disorders. 4 key findings →
Design: cross-sectional
Participants: 81
Evidence: moderate
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Neurofilament light (NfL) is a marker of neuroaxonal injury, a prominent feature of Alzheimer's disease. 4 key findings →
Design: cross-sectional
Participants: 1,149
Evidence: moderate
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Higher levels of P-tau181 (HR = 1.32 [95% CI: 1.17-1.51]), NfL (HR = 1.19 [95% CI: 1.03-1.36]), and GFAP (HR = 1.36 [95% CI: 1.22-1.52]), and a lower Aβ42/Aβ40 ratio (HR = 0.80 [95% CI: 0.68-0.95]) were associated with an increased risk of progressing to clinically-diagnosed DAT. 2 key findings →
Design: longitudinal study
Participants: 1,007
Evidence: moderate
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64/100
✓ Peer-reviewed
alzhub usefulness score 64 out of 100.
·
Neurology
·
2026-07-13
Prion diseases can mimic Alzheimer disease (AD) at presentation. 4 key findings →
Design: cohort study
Participants: 345
Evidence: moderate
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Studies evaluating the diagnostic test accuracy of plasma phosphorylated tau (p-tau) and amyloid beta (Aβ) tests (p-tau217, %p-tau217, p-tau181, p-tau231, and Aβ42/Aβ40) compared to reference standard tests (cerebrospinal fluid [CSF] AD biomarkers, amyloid positron emission tomography [PET], or neuropathology) in individuals with cognitive impairment (mild cognitive impairment or dementia) in specialized care settings were included. 4 key findings →
Design: meta-analysis
Evidence: moderate
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We enrolled a cohort of 1070 PSEN1 E280A mutation carriers and 1074 non-carriers with baseline assessments; of these participants, longitudinal measures (with a mean follow-up of 6 years) were available for 242 mutation carriers and 262 non-carriers. 1 key finding →
Design: cohort study
Evidence: moderate
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Disease-modifying therapies for Alzheimer's disease (AD) are likely to be most beneficial when initiated in the presymptomatic phase. 2 key findings →
Design: cross-sectional
Participants: 567
Evidence: moderate
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63/100
✓ Peer-reviewed
alzhub usefulness score 63 out of 100.
·
JAMA network open
·
2025-03-03
These findings suggest that PA may help delay cognitive decline by modulating neurodegeneration and AD-specific tau pathologies. 4 key findings →
Design: cross-sectional
Participants: 1,144
Evidence: moderate
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63/100
✓ Peer-reviewed
alzhub usefulness score 63 out of 100.
·
Brain
·
2025-10-03
Using the Swedish BioFINDER-2 cohort [n = 1702, 50.7% male, mean (standard deviation) age 68.4 (12.2) years], we compared the associations between tau/Aβ-PET load and fluid biomarkers alone versus biomarkers in a ratio with a reference protein (Aβ40 or np-tau) in univariate linear regression models. 5 key findings →
Design: longitudinal study
Participants: 1,702
Evidence: moderate
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62/100
✓ Peer-reviewed
alzhub usefulness score 62 out of 100.
·
JAMA network open
·
2025-05-01
Lobar CMB counts and the presence of CAA were associated with downstream AD plasma biomarkers, including p-tau217 (β = 0.12 [95% CI, 0.05-0.18] and 0.29 [95% CI, 0.12-0.47], respectively), GFAP (β = 0.07 [95% CI, 0.03-0.12] and 0.20 [95% CI, 0.09-0.31], respectively), and NfL (β = 0.07 [95% CI, 0.03-0.11] and 0.16 [95% CI, 0.06-0.25], respectively) with and without the mediation of Aβ uptake on PET (indirect effect: lobar CMBs-p-tau217, 59.8% [β = 0.07 (95% CI, 0.03-0.11)]; lobar CMBs-GFAP, 49.3% [β = 0.04 (95% CI, 0.01-0.06)]; lobar CMBs-NfL, 20.9% [β = 0.01 (95% CI, 0.01-0.03)]; CAA-p-tau217, 50.9% [β = 0.15 (95% CI, 0.06-0.24)]; CAA-GFAP, 39.2% [β = 0.08 (95% CI, 0.03-0.13)]; CAA-NfL, 19.2% [β = 0.03 (95% CI, 0.01-0.05)]). 4 key findings →
Design: cohort study
Participants: 1,708
Evidence: moderate
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Alzheimer's disease (AD) is a progressive neurodegenerative disease with a complex and heterogeneous pathophysiology. 4 key findings →
Evidence: low
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Plasma markers of inflammation and complement dysregulation support diagnosis and outcome prediction in AD and MCI. 1 key finding →
Evidence: moderate
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61/100
✓ Peer-reviewed
alzhub usefulness score 61 out of 100.
·
Nature Medicine
·
2007-10-14
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60/100
✓ Peer-reviewed
alzhub usefulness score 60 out of 100.
·
JAMA network open
·
2023-11-01
These findings suggest that increases in certain plasma AD biomarkers are associated with NP in WLWH and WLWOH and may be associated with later onset of AD, and measuring these biomarkers could be a pivotal advancement in monitoring aging brain health and development of AD among women with and without HIV. 5 key findings →
Design: cohort study
Participants: 307
Evidence: moderate
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60/100
✓ Peer-reviewed
alzhub usefulness score 60 out of 100.
·
Neurology
·
2025-10-17
The aim of this study was to evaluate longitudinal associations of multimodal core 1 AD biomarkers with cognition in a cognitively unimpaired (CU) population at increased risk of AD dementia. 4 key findings →
Design: longitudinal study
Participants: 350
Evidence: moderate
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59/100
✓ Peer-reviewed
alzhub usefulness score 59 out of 100.
·
Annals of surgery
·
2019-06-01
Delirium following surgery is common and associated with adverse outcomes. 2 key findings →
Design: cohort study
Participants: 282
Evidence: moderate
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During follow-up, 57 (42%) patients with MCI developed Alzheimer's disease, 21 (15%) developed other forms of dementia, and 56 (41%) remained cognitively stable for 5.2 years (range 4.0-6.8). 1 key finding →
Evidence: low
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A growing body of evidence suggests that the plasma concentration of the neurofilament light chain (NfL) might be considered a plasma biomarker for the screening of neurodegeneration in Alzheimer's disease (AD). 4 key findings →
Participants: 25
Evidence: low
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58/100
✓ Peer-reviewed
alzhub usefulness score 58 out of 100.
·
Neurology
·
2022-05-26
The proposed novel, pragmatic method to determine CSF biomarker cutoffs for AD does not require assessment of other biomarkers or assumptions concerning the clinical diagnosis of patients. 1 key finding →
Participants: 497
Evidence: low
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-fold changes of 1.21, 0.57, and 4.63, respectively, compared to A-. 5 key findings →
Design: cross-sectional
Participants: 252
Evidence: low
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A total of 1,345 individuals were included. 5 key findings →
Design: cohort study
Participants: 1,345
Evidence: moderate
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This study reviewed the structure, function, analytical aspects, and age-dependent normal ranges of neurofilaments, providing a comprehensive overview of neurofilament light chain as a marker of axonal injury across various neurological disorders. 2 key findings →
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57/100
✓ Peer-reviewed
alzhub usefulness score 57 out of 100.
·
Nature Aging
·
2026-02-13
Dementia diagnosis increasingly relies on blood-based biomarkers, yet their performance in diverse populations remains insufficiently characterized. 1 key finding →
Design: cross-sectional
Participants: 605
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
- Randomized / 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
- Multicenter 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 32,180 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.