Our results demonstrated that dual-task could significantly improve the ability to predict cognitive impairment based on gait parameters such as gait speed (GS) and stride length (SL). 5 key findings →
Participants: 38
Evidence: low
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BackgroundEarly diagnosis of early-onset dementia (EOD) is often challenging. 1 key finding →
Participants: 54
Evidence: low
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We selected 111 patients with probable DLB and CSF available from the Amsterdam Dementia Cohort. 4 key findings →
Participants: 111
Evidence: moderate
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BackgroundCognitive impairment significantly impacts the quality of life in patients with neurodegenerative disorders, including Huntington's disease (HD), Parkinson's disease (PD), and Alzheimer's disease (AD).ObjectiveThis study aims to assess the utility of MemTrax, a contemporary digital continuous recognition task platform originally developed for AD, as an effective tool for revealing cognitive and clinical motor impairments in HD and PD populations as aligned with respective disease staging. 2 key findings →
Participants: 135
Evidence: low
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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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The combination of MemTrax and BBMs provides an accurate, convenient, non-invasive, cost-effective and scalable way to estimate Aβ load, which provides an opportunity for mass screening and timely and accurate diagnosis of AD. 3 key findings →
Participants: 349
Evidence: low
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Low n-3 polyunsaturated fatty acid (PUFA) status may be associated with neuro-degenerative disorders, in particular Alzheimer's disease, which has been associated with poor dietary fish or n-3 PUFA intake, and low docosahexaenoic acid (DHA) status. 4 key findings →
Design: case-control study
Evidence: moderate
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The BHA measures are significantly associated with both Aβ and regional tau in vivo imaging markers and could be used for the identification of patients with suspected AD pathology in clinical practice. 3 key findings →
Participants: 140
Evidence: low
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52/100
✓ Peer-reviewed
alzhub usefulness score 52 out of 100.
·
Gerontology
·
2024-01-12
Our research proposes that reading-derived speech data facilitates the differentiation between cognitively impaired individuals and cognitively intact, age-matched older adults. 4 key findings →
Participants: 59
Evidence: low
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In the ADMET2 biomarker subset (n = 44, MPH:21, age:75 years, MMSE:20.2), higher baseline TNF was associated with higher M6 NPI-A [B(SE)= 6.86 (1.71), p = .0003], and multivariable models found lower baseline TNF [B(SE)= 8.28(1.61), p < .001] and higher baseline S100B [B(SE)= -6.41(1.95), p = .002] were associated with lower M6 NPI-A. Exploratory analyses suggested that higher baseline NfL significantly interacted with treatment to predict lower M6 NPI-A [B(SE)= -8.36(4.21), p = .05], only when adjusting for cognition. 5 key findings →
Participants: 44
Evidence: high
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Disease-modifying treatment trials are increasingly advanced to the prodromal or preclinical phase of Alzheimer's disease (AD), and inclusion criteria are based on biomarkers rather than clinical symptoms. 4 key findings →
Participants: 13
Evidence: low
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Elevated CSF τ is considered a biomarker of neuronal injury in newly developed Alzheimer's disease (AD) and mild cognitive impairment (MCI) criteria. 4 key findings →
Participants: 24
Evidence: low
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A total of 101 FTD patients (64 ± 8 years, 53 men), 230 AD patients (65 ± 10 years, 84 men), and 173 CTR (59 ± 15 years, 67 men) were studied. 5 key findings →
Design: cross-sectional
Participants: 101
Evidence: moderate
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Our results suggest that the ki:e SB-C is an objective, scalable, and reliable indicator of cognitive decline, fit for purpose as a remote assessment in clinical early dementia trials. 3 key findings →
Participants: 69
Evidence: low
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Both DELPHI analysis of network function and DTI analysis detected a significant decrease in connectivity, excitability, and WM integrity in the SCD group compared to healthy control (HC) subjects; a significant decrease was also noted for aMCI and Dementia groups compared to HC. 3 key findings →
Participants: 17
Evidence: low
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Biomarkers play an important role in Alzheimer's disease (AD) clinical trials in several contexts of use, including defining trial eligibility and serving as outcome measures. 5 key findings →
Design: clinical trial
Evidence: low
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The association of alpha-synuclein (alpha-syn) neuropathology with Parkinson's disease (PD) and several related disorders has led to an intense research effort to develop cerebrospinal fluid (CSF)- or blood-based alpha-syn biomarkers for these types of diseases. 4 key findings →
Participants: 15
Evidence: low
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Cerebrospinal fluid (CSF) concentrations of tau protein were measured using an enzyme-linked immunosorbent assay which measures both normal and hyperphosphorylated tau. 4 key findings →
Participants: 17
Evidence: low
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Soluble N-ethylmaleimide-sensitive factor attachment proteins receptors (SNARE) proteins, such as VAMP-2 and SNAP-25, are implicated in α-synuclein pathophysiology and CSF levels of these proteins are associated with pathophysiological biomarkers and cognitive decline in Alzheimer’s disease (AD). 5 key findings →
Participants: 62
Evidence: moderate
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Moreover, we found, in either the whole AD population or both subgroups, a CSF profile in which higher 4 key findings →
Participants: 145
Evidence: low
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Decades of research has established a shift from an "eveningness" preference to a "morningness" preference with increasing age. 4 key findings →
Participants: 169
Evidence: low
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The use and evaluation of digital biomarkers, objective and quantifiable measures of biology, and health collected through digital devices is growing rapidly. 5 key findings →
Participants: 1,290
Evidence: low
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These findings suggest that AD biomarker levels may be differentially predictive of specific cognitive functions many years later. 5 key findings →
Participants: 67
Evidence: moderate
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This study demonstrated DCBs' ability to distinguish , at baseline, between impending cognitive decline and non-decline groups where individuals in both groups were classified as cognitively normal. 5 key findings →
Participants: 61
Evidence: low
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Oculomotor abnormalities are a common finding in neurodegenerative diseases due to degeneration of neural pathways and brain regions involved in controlling eye movements. 5 key findings →
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
- 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 31,380 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.