53/100
✓ Peer-reviewed
alzhub usefulness score 53 out of 100.
·
Neurology
·
2020-09-01
Cross-sectional data, including CSF analytes, molecular imaging of cerebral fibrillar β-amyloid (Aβ) with PET using the [ 11 C] benzothiazole tracer Pittsburgh compound B (PiB), MRI-based brain structures, and clinical/cognitive outcomes harmonized from 8 studies, collectively involving 3,284 cognitively normal individuals 18 to 101 years of age, were analyzed. 4 key findings →
Design: cross-sectional
Evidence: low
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53/100
✓ Peer-reviewed
alzhub usefulness score 53 out of 100.
·
Neurology
·
2023-05-18
White matter hyperintensities (WMH) correlate with Alzheimer disease (AD) biomarkers cross-sectionally and modulate AD pathogenesis. 4 key findings →
Design: longitudinal study
Evidence: moderate
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To explore markers for synaptic function and Alzheimer disease (AD) pathology in late life depression (LLD), predementia AD and normal controls (NC). 4 key findings →
Design: cross-sectional
Participants: 16
Evidence: low
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Altered levels of kynurenines in blood and cerebrospinal fluid (CSF) have been reported in Alzheimer's disease (AD). 4 key findings →
Design: cohort study
Participants: 138
Evidence: moderate
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53/100
✓ Peer-reviewed
alzhub usefulness score 53 out of 100.
·
Neurology
·
2025-11-17
α-Synuclein (αSyn) seed amplification assays (SAAs) accurately detect αSyn pathology in dementia with Lewy bodies (DLB). 4 key findings →
Design: cohort study
Evidence: moderate
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53/100
✓ Peer-reviewed
alzhub usefulness score 53 out of 100.
·
JAMA network open
·
2026-08-03
Moreover, there is limited knowledge regarding associations with domain-specific cognitive decline and modifying effects of key individual characteristics. 4 key findings →
Design: cohort study
Participants: 2,008
Evidence: moderate
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53/100
✓ Peer-reviewed
alzhub usefulness score 53 out of 100.
·
Neurology
·
2026-08-04
Late-onset unexplained epilepsy (LOUE) represents a substantial proportion of epilepsies with onset after 50 years and often manifests as temporal lobe epilepsy (LO-TLE). 4 key findings →
Design: cohort study
Participants: 18
Evidence: moderate
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Low levels of cerebrospinal fluid (CSF) beta-amyloid 1-42 (Abeta42) and high total tau (T-tau) are diagnostic for manifest Alzheimer's disease. 4 key findings →
Design: longitudinal study
Evidence: moderate
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For amyloid positive individuals Aβ42/Aβ40, glial fibrillary acidic protein and p-tau181 were the top predictors of cognitive decline while Aβ42/Aβ40 was prominent for amyloid negative participants across all age groups. 5 key findings →
Design: cross-sectional
Participants: 1,185
Evidence: moderate
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The complexity of neurodegenerative disorders necessitates an integrative approach that incorporates morphological, functional, and molecular biomarkers. 3 key findings →
Participants: 279
Evidence: moderate
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52/100
✓ Peer-reviewed
alzhub usefulness score 52 out of 100.
·
JAMA Network Open
·
2026-08-03
Among 356 patients (79%) with AD as the primary suspected etiology, assessment of BBM classified 149 patients (42%) as high, 101 patients (28%) as intermediate, and 106 patients (30%) as low probability of AD. 5 key findings →
Design: cohort
Participants: 450
Evidence: moderate
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Plasma phosphorylated tau (p-tau)181, glial fibrillary acidic protein (GFAP), neurofilament light chain (NfL), and amyloid beta ratio (Aβ42/40) may have diagnostic and prognostic value in Alzheimer's disease (AD). 2 key findings →
Design: cross-sectional
Participants: 1,298
Evidence: moderate
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Cerebrospinal fluid analyses and neuroimaging can identify the underlying pathophysiology at the earliest stage of some neurodegenerative disorders, but do not have the scalability needed for population screening. 5 key findings →
Evidence: low
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52/100
✓ Peer-reviewed
alzhub usefulness score 52 out of 100.
·
Anesthesiology
·
2016-02-01
Low CSF Aβ1-42 may be a significant predictor of POCD at 3 months. 5 key findings →
Participants: 59
Evidence: low
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52/100
✓ Peer-reviewed
alzhub usefulness score 52 out of 100.
·
Neurology
·
2015-10-14
Amyloid-PET-based CSF Aβ42 cutpoints were higher and tended to reduce intercenter variability compared with clinical-based cutpoints. 3 key findings →
Participants: 433
Evidence: moderate
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52/100
✓ Peer-reviewed
alzhub usefulness score 52 out of 100.
·
Autophagy
·
2024-05-02
Defective mitophagy is consistently found in postmortem brain and iPSC-derived neurons from Alzheimer disease (AD) patients. 1 key finding →
Participants: 100
Evidence: low
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Importantly, Aβ42/Aβ40 ratio remained unaltered, suggesting that it is more suitable for implementation in clinical workup than individual Aβ peptides. 4 key findings →
Participants: 20
Evidence: low
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The therapeutic imperative for Alzheimer disease (AD) and Parkinson disease (PD) calls for discovery and validation of biomarkers. 5 key findings →
Participants: 48
Evidence: low
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52/100
✓ Peer-reviewed
alzhub usefulness score 52 out of 100.
·
Neurology
·
2012-04-18
Amyloid plaques and hyperphosphorylated tau in cortical brain biopsies are reflected by low CSF Aβ42 and high CSF tau and p-tau levels, respectively. 2 key findings →
Participants: 182
Evidence: low
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Olfactory identification deficit is a useful screening tool for AD-related amnestic disorder, with sensitivity and specificity comparable to other established biomarkers, with benefits such as ease of administration and low cost. 1 key finding →
Design: cross-sectional
Participants: 96
Evidence: moderate
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A number of in vivo neurochemistry and neuroimaging techniques, which can reliably assess aspects of physiology, pathology, chemistry, and neuroanatomy, hold promise as biomarkers. 2 key findings →
Evidence: low
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Dementia is a global epidemic with Alzheimer's disease (AD) being the leading cause. 3 key findings →
Participants: 273
Evidence: moderate
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Proteomic studies for Alzheimer's disease (AD) are instrumental in identifying AD pathways but often focus on single tissues and sporadic AD cases. 4 key findings →
Evidence: low
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Cerebrospinal fluid (CSF) concentrations of amyloid beta peptides ending at positions 42 and 40 (Abeta42 and Abeta40, respectively), and total tau (tTau) protein were measured by ELISA in order to compare their accuracy in discriminating patients with Alzheimer's disease (AD, n = 22), non-Alzheimer dementia (nAD, n = 11) and control subjects (CON, n=35). 4 key findings →
Participants: 22
Evidence: low
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52/100
✓ Peer-reviewed
alzhub usefulness score 52 out of 100.
·
Neurology
·
2009-10-01
CSF biomarkers amyloid beta 1-42 (Abeta(42)), total tau (tau), and tau phosphorylated at threonine 181 (p-tau-181) are useful diagnostic markers for Alzheimer disease (AD). 4 key findings →
Participants: 151
Evidence: low
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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.