Key points • Decreasing CBF relates to more advanced AD stages in all supratentorial regions. • The reduction of CBF does not reach a bottom level. • ASL-CBF has potential as a measure for disease progression in AD. 1 key finding →
Participants: 177
Evidence: moderate
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53/100
✓ Peer-reviewed
alzhub usefulness score 53 out of 100.
·
Neurology
·
2017-09-08
Using a cross-sectional design, we examined retinal structure in 38 consecutively enrolled patients with FTD and 44 controls using a standard SD-OCT protocol. 4 key findings →
Design: cross-sectional
Participants: 46
Evidence: low
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53/100
✓ Peer-reviewed
alzhub usefulness score 53 out of 100.
·
Aging
·
2022-02-07
In humans, aging, triggers increased plasma concentrations of triglycerides, cholesterol, low-density lipoproteins and lower capacity of high-density lipoproteins to remove cellular cholesterol. 4 key findings →
Design: cohort study
Evidence: moderate
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According to the vascular depression hypothesis, subclinical cerebrovascular disease can cause depression in older adults. 4 key findings →
Design: cross-sectional
Participants: 1,494
Evidence: moderate
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53/100
✓ Peer-reviewed
alzhub usefulness score 53 out of 100.
·
NeuroImage
·
2019-03-04
Current models of progression in neurodegenerative diseases use neuroimaging measures that are averaged across pre-defined regions of interest (ROIs). 4 key findings →
Design: longitudinal study
Evidence: moderate
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53/100
✓ Peer-reviewed
alzhub usefulness score 53 out of 100.
·
Theranostics
·
2020-01-01
Microglial activation participates in white matter injury after cerebral hypoperfusion. 4 key findings →
Participants: 80
Evidence: low
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In linear mixed models, vascular endothelial growth factor was significantly associated with incident DWI-positive lesions over 1 year. 5 key findings →
Design: cross-sectional
Participants: 181
Evidence: moderate
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The final model, which included age, systolic blood pressure >140, atrial fibrillation, and tobacco use, achieved an AUC of 0.83 (95% CI 0.75-0.90) in the development cohort (N=143, 62.4±12.6 years, 44% female, 36% non-white race) and 0.85 (95% CI 0.77-0.92) in the validation cohort (N=127, 65.2±16.8 years, 51% female, 34% non-white race), with similar results using WMH measurements derived from cMRI (N=120, p=0.98, AUC=0.86, 95% CI 0.77-0.93). 5 key findings →
Participants: 143
Evidence: moderate
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Cohort 1 included 446 individuals (mean age (SD) 65.2 years (8.9); 203 women), Cohort 2 included 164 individuals (mean age (SD) 49.9 years (12.6); 88 women). 5 key findings →
Design: longitudinal study
Participants: 446
Evidence: moderate
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53/100
✓ Peer-reviewed
alzhub usefulness score 53 out of 100.
·
Hypertension
·
2025-10-29
In SPRINT, the overall interaction between age and SBP on WMHv change was not statistically significant ( P =0.18). 5 key findings →
Design: longitudinal study
Participants: 172
Evidence: moderate
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A total of 261 patients (75.3±6.8 years) were recruited from a memory-clinic cohort. 5 key findings →
Design: cross-sectional
Participants: 261
Evidence: moderate
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Twenty-four patients of comparable age, blood pressure, and degree of dementia were classified by an "Ischemic Score" based on clinical features into "multi-infarct" and "primary degenerative" dementia. 5 key findings →
Evidence: low
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Traumatic brain injury (TBI), a major cause of persistent cognitive impairment (CI), increases the long-term risk of developing dementia, including Alzheimer's disease (AD). 3 key findings →
Design: longitudinal study
Participants: 29
Evidence: moderate
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Neurogranin (Ng) is a post-synaptic protein that previously has been shown to be a biomarker for synaptic function when measured in cerebrospinal fluid (CSF). 5 key findings →
Participants: 915
Evidence: low
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Neurodegenerative diseases likely share common underlying pathobiology. 5 key findings →
Participants: 82,337
Evidence: low
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The blood-brain barrier (BBB) is a complex and dynamic physiological interface between brain parenchyma and cerebral vasculature. 1 key finding →
Design: longitudinal study
Evidence: moderate
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Cerebral white matter lesions (WML) encompass axonal loss and demyelination and are assumed to be associated with small vessel disease (SVD)-related ischaemia. 5 key findings →
Participants: 19
Evidence: low
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Accumulating evidence implicates small vessel cerebrovascular disease, visualized as white matter hyperintensities (WMH) on T2-weighted magnetic resonance imaging, in the pathogenesis and diagnosis of Alzheimer's disease (AD). 2 key findings →
Design: cross-sectional
Participants: 26
Evidence: moderate
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52/100
✓ Peer-reviewed
alzhub usefulness score 52 out of 100.
·
Circulation
·
2010-08-02
Although observational data cannot establish causality, our findings are consistent with the hypothesis that decreasing cardiac function, even at normal cardiac index levels, is associated with accelerated brain aging. 5 key findings →
Evidence: moderate
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Stepwise decreases in WM integrity as measured by both DTI and FLAIR were independently associated with stepwise increases in WMH risk, emphasizing that these modalities may provide complementary information for understanding the time course of aging-associated WM degeneration. 3 key findings →
Design: longitudinal study
Evidence: moderate
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This human study is based on an established cohort of "SuperAgers," 80+-year-old individuals with episodic memory function at a level equal to, or better than, individuals 20-30 years younger. 4 key findings →
Participants: 21
Evidence: moderate
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The presence of either severe WMH or MTA was associated with a modest but non-significant increase in frequency of mild cognitive deficits (severe WMH: odds ratio (OR) = 1.9 (95% confidence interval (CI), 1.0 to 3.7); MTA present: OR = 1.5 (95% CI, 0.8 to 2.8)). 2 key findings →
Participants: 639
Evidence: low
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52/100
✓ Peer-reviewed
alzhub usefulness score 52 out of 100.
·
Stroke
·
2016-04-07
The prevalence of ICAS in older adults is high, and it could be a target for primary prevention of stroke and dementia in this population. 3 key findings →
Participants: 1,765
Evidence: moderate
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Epidemiologic data suggest that individuals at all stages of CKD have a higher risk of developing cognitive disorders and dementia. 1 key finding →
Evidence: low
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Wakefulness, along with fast cortical rhythms and associated cognition, depend on the basal forebrain (BF). 3 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
- 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.