ReviewMolecular neurodegeneration2018
Disease-modifying effects of metabolic perturbations in ALS/FTLD.
Review in Molecular neurodegeneration, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
What it found
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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
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.
- Diabetes Mellitus and Amyotrophic Lateral Sclerosis: A Systematic Review.Biomolecules · 2021Pooled it
- Neuronal Cell-Cycle Re-entry Defines Divergent Outcomes Through Replication-Dependent DNA Damage in ALS.bioRxiv : the preprint server for biology · 2026Article
- Targeting Multilayered Metabolic Networks in Brain Diseases: Emerging Perspectives on Nanodelivery Strategies.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Neuroprotective Effect of a Multistrain Probiotic Mixture in SOD1Molecular neurobiology · 2024Article
- Lifestyle and medical conditions in relation to ALS risk and progression-an introduction to the Swedish ALSrisc Study.Journal of neurology · 2024Article
- Higher Glycemic Index and Glycemic Load Diet Is Associated with Slower Disease Progression in Amyotrophic Lateral Sclerosis.Annals of neurology · 2024Article
- Metabolic Disturbances in a Mouse Model of MPTP/Probenecid-Induced Parkinson's Disease: Evaluation Using Liquid Chromatography-Mass Spectrometry.Neuropsychiatric disease and treatment · 2024Article
- Mutation in the FUS nuclear localisation signal domain causes neurodevelopmental and systemic metabolic alterations.Disease models & mechanisms · 2023Article
- Improvement in Zebrafish with Diabetes and Alzheimer's Disease Treated with Pasteurized Akkermansia muciniphila.Microbiology spectrum · 2023Article
- APOE2 Exacerbates TDP-43 Related Toxicity in the Absence of Alzheimer Pathology.Annals of neurology · 2023Article
- Fatty acids derived from the probiotic Lacticaseibacillus rhamnosus HA-114 suppress age-dependent neurodegeneration.Communications biology · 2022Article
- Activation of the Mitochondrial Unfolded Protein Response: A New Therapeutic Target?Biomedicines · 2022Review
- TDP-43 regulates cholesterol biosynthesis by inhibiting sterol regulatory element-binding protein 2.Scientific reports · 2022Article
- Mitochondrial dysregulation occurs early in ALS motor cortex with TDP-43 pathology and suggests maintaining NADScientific reports · 2022Article
- Adiponectin-mimetic novel nonapeptide rescues aberrant neuronal metabolic-associated memory deficits in Alzheimer's disease.Molecular neurodegeneration · 2021Article
- Comprehensive metabolic profiling of Parkinson's disease by liquid chromatography-mass spectrometry.Molecular neurodegeneration · 2021Article
- Disruption of Endoplasmic Reticulum Proteostasis in Age-Related Nervous System Disorders.Progress in molecular and subcellular biology · 2021Article
- Trends in Understanding the Pathological Roles of TDP-43 and FUS Proteins.Advances in experimental medicine and biology · 2021Article
- Brain energy rescue: an emerging therapeutic concept for neurodegenerative disorders of ageing.Nature reviews. Drug discovery · 2020Review
- From basic research to the clinic: innovative therapies for ALS and FTD in the pipeline.Molecular neurodegeneration · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD) are two fatal neurodegenerative disorders with considerable clinical, pathological and genetic overlap. Both disorders are characterized by the accumulation of pathological protein aggregates that contain a number of proteins, most notably TAR DNA binding protein 43 kDa (TDP-43). Surprisingly, recent clinical studies suggest that dyslipidemia, high body mass index, and type 2 diabetes mellitus are associated with better clinical outcomes in ALS. Moreover, ALS and FTLD patients have a significantly lower incidence of cardiovascular disease, supporting the idea that an unfavorable metabolic profile may be beneficial in ALS and FTLD. The two most widely studied ALS/FTLD models, super-oxide dismutase 1 (SOD1) and TAR DNA binding protein of 43 kDA (TDP-43), reveal metabolic dysfunction and a positive effect of metabolic strategies on disease onset and/or progression. In addition, molecular studies reveal a role for ALS/FTLD-associated proteins in the regulation of cellular and whole-body metabolism. Here, we systematically evaluate these observations and discuss how changes in cellular glucose/lipid metabolism may result in abnormal protein aggregations in ALS and FTLD, which may have important implications for new treatment strategies for ALS/FTLD and possibly other neurodegenerative conditions.
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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.