Our study is not subject to the biases of meta-analyses of published data, and it represents an important milestone in an ongoing collaborative effort to examine the neurobiological underpinnings of PTSD and the brain's response to trauma. 2 key findings →
Design: meta-analysis
Participants: 1,868
Evidence: high
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Relative to control subjects, patients had significantly smaller HCVs (standardized mean difference = -0.32 [95% confidence interval, -0.44 to -0.19]). 5 key findings →
Design: cohort study
Participants: 2,702
Evidence: moderate
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The negative association between depression treatment and incident dementia was significant in the increasing and chronically low courses, highlighting the necessity of timely interventional strategies before depression progresses to a chronically severe state. 4 key findings →
Design: cohort
Participants: 354,313
Evidence: moderate
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We demonstrate that using additional phenotype data previously collected by genetic studies to tackle phenotypic heterogeneity in MDD can successfully lead to the discovery of genetic risk factor despite reduced sample size. 5 key findings →
Design: meta-analysis
Evidence: high
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We tested the hypothesis that a causal relationship exists between systolic BP (SBP) and/or diastolic BP (DBP) and risk of Alzheimer's disease (AD). 4 key findings →
Design: meta-analysis
Participants: 299,024
Evidence: high
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The number of ECT sessions and electrode placement impacts the extent and laterality of hippocampal enlargement, but volume change is not positively associated with clinical outcome. 4 key findings →
Design: longitudinal study
Participants: 281
Evidence: moderate
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These results strengthen the clinical evidence that AD is accompanied by an inflammatory response, particularly higher peripheral concentrations of IL-6, TNF-α, IL-1β, TGF-β, IL-12 and IL-18 and higher CSF concentrations of TGF-β. 5 key findings →
Participants: 680
Evidence: low
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Long-term exposure to PM 2.5 contributed to the development of cognitive decline, which may be partly explained by brain amyloid accumulation indicative of increased AD risk. 1 key finding →
Design: cross-sectional
Participants: 31,573
Evidence: moderate
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Sodium benzoate substantially improved cognitive and overall functions in patients with early-phase AD. 3 key findings →
Evidence: high
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Obesity and diabetes significantly and independently increase risk for AD. 5 key findings →
Design: meta-analysis
Evidence: high
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These data demonstrate that YKL-40, a putative indicator of neuroinflammation, is elevated in AD and, together with Aβ42, has potential prognostic utility as a biomarker for preclinical AD. 3 key findings →
Participants: 47
Evidence: moderate
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Elevated preoperative and postoperative plasma levels of C-reactive protein were associated with delirium, suggesting that a preinflammatory state and heightened inflammatory response to surgery are potential pathophysiologic mechanisms of delirium. 4 key findings →
Design: case-control study
Participants: 566
Evidence: moderate
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Although numerous studies of the longitudinal course of schizophrenia have demonstrated the clinical deterioration that occurs predominantly in the early stages of the illness, the pathophysiology of this clinical phenomenon has not been established. 5 key findings →
Design: longitudinal study
Participants: 107
Evidence: moderate
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There is a growing literature on the importance of hippocampal volume in geriatric depression. 4 key findings →
Design: longitudinal study
Participants: 66
Evidence: moderate
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Plasma BACE1 activity is significantly increased in MCI converters and patients with probable AD. 5 key findings →
Participants: 96
Evidence: low
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We review the genetic risk factors for late-onset Alzheimer's disease (AD) and their role in AD pathogenesis. 4 key findings →
Evidence: low
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These results suggest that bvFTD may be characterized by an allostatic-interoceptive overload manifested in ongoing electrophysiological markers, brain atrophy, functional networks, and cognition. 4 key findings →
Participants: 94
Evidence: low
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Traumatic brain injury (TBI), particularly of greater severity (i.e., moderate to severe), has been identified as a risk factor for all-cause dementia and Parkinson's disease, with risk for specific dementia subtypes being more variable. 1 key finding →
Evidence: low
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Thirty-three percent of LLD participants met ADNI criteria for mild cognitive impairment. 4 key findings →
Participants: 119
Evidence: low
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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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ECT-induced neuroplasticity in the hippocampus and amygdala relates to improved clinical response and is pronounced in regions with prominent connections to ventromedial prefrontal cortex and other limbic structures. 2 key findings →
Design: cross-sectional
Participants: 43
Evidence: moderate
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Visual impairment and interventions to preserve vision may impact dementia risk. 4 key findings →
Participants: 300,823
Evidence: low
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Smaller hippocampal volume in adolescents at high risk for depression suggests that it may be a vulnerability marker for the illness. 4 key findings →
Design: longitudinal study
Evidence: moderate
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Future longitudinal studies with trauma control subjects and neuropsychological measures are indicated to further elucidate the relationship between hippocampus and behavioral abnormalities in young PTSD subjects. 3 key findings →
Design: longitudinal study
Evidence: moderate
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Individuals with AD were clustered into 4 subtypes reproducibly, which included those with 1) diffuse and mild functional connectivity disruption (subtype 1), 2) predominantly decreased connectivity in the default mode network accompanied by an increase in the prefrontal circuit (subtype 2), 3) predominantly decreased connectivity in the anterior cingulate cortex accompanied by an increase in prefrontal cortex connectivity (subtype 3), and 4) predominantly decreased connectivity in the basal ganglia accompanied by an increase in prefrontal cortex connectivity (subtype 4). 3 key findings →
Participants: 809
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.