ReviewFrontiers in neuroscience2015
Integrative neurobiology of metabolic diseases, neuroinflammation, and neurodegeneration.
Review in Frontiers in neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
44 citing papers in PubMed, 2 syntheses or guidelines pooled it, 71 citations in OpenAlex.
- Postmortem evidence of cerebral inflammation in schizophrenia: a systematic review.Molecular psychiatry · 2016Pooled it
- Current status of PET imaging in Huntington's disease.European journal of nuclear medicine and molecular imaging · 2016Pooled it
- Time-restricted feeding in adult mice improves mood-related behaviors in a sex-dependent manner.Behavioural brain research · 2026Article
- Systemic TGF-β1 reduction contributes to neuronal GLUT4 trafficking impairment in acute hepatic encephalopathy.Frontiers in molecular neuroscience · 2026Article
- TNF as a mediator of metabolic inflammation and body-brain interaction in obesity-driven neuroinflammation and neurodegeneration.Ageing research reviews · 2025Review
- Sex differences in the effects of high fat diet on underlying neuropathology in a mouse model of VCID.Biology of sex differences · 2023Article
- Thyroid Function and Metabolic Syndrome in Children and Adolescents with Neuromotor Disability.Children (Basel, Switzerland) · 2022Article
- Targeting hypercoagulation to alleviate Alzheimer's disease progression in metabolic syndrome.International journal of obesity (2005) · 2022Review
- Garlic exosome-like nanoparticles reverse high-fat diet induced obesity via the gut/brain axis.Theranostics · 2022Article
- Current Trends in Neurodegeneration: Cross Talks between Oxidative Stress, Cell Death, and Inflammation.International journal of molecular sciences · 2021Review
- Article
- Tibolone Ameliorates the Lipotoxic Effect of Palmitic Acid in Normal Human Astrocytes.Neurotoxicity research · 2020Article
- Obstructive Sleep Apnea in Neurodegenerative Disorders: Current Evidence in Support of Benefit from Sleep Apnea Treatment.Journal of clinical medicine · 2020Review
- Deciphering the Role of WNT Signaling in Metabolic Syndrome-Linked Alzheimer's Disease.Molecular neurobiology · 2020Review
- Targeting soluble tumor necrosis factor as a potential intervention to lower risk for late-onset Alzheimer's disease associated with obesity, metabolic syndrome, and type 2 diabetes.Alzheimer's research & therapy · 2019Article
- Chronic inflammation in the etiology of disease across the life span.Nature medicine · 2019Review
- Mechanisms Associated with Type 2 Diabetes as a Risk Factor for Alzheimer-Related Pathology.Molecular neurobiology · 2019Article
- Association of plasma endothelial lipase levels on cognitive impairment.BMC psychiatry · 2019Article
- Article
- G Protein-Coupled Receptor Systems as Crucial Regulators of DNA Damage Response Processes.International journal of molecular sciences · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is a complex, multifactorial disease with a number of leading mechanisms, including neuroinflammation, processing of amyloid precursor protein (APP) to amyloid β peptide, tau protein hyperphosphorylation, relocalization, and deposition. These mechanisms are propagated by obesity, the metabolic syndrome and type-2 diabetes mellitus. Stress, sedentariness, dietary overconsumption of saturated fat and refined sugars, and circadian derangements/disturbed sleep contribute to obesity and related metabolic diseases, but also accelerate age-related damage and senescence that all feed the risk of developing AD too. The complex and interacting mechanisms are not yet completely understood and will require further analysis. Instead of investigating AD as a mono- or oligocausal disease we should address the disease by understanding the multiple underlying mechanisms and how these interact. Future research therefore might concentrate on integrating these by "systems biology" approaches, but also to regard them from an evolutionary medicine point of view. The current review addresses several of these interacting mechanisms in animal models and compares them with clinical data giving an overview about our current knowledge and puts them into an integrated framework.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.