ReviewNeuroSci2024
Trehalose: Neuroprotective Effects and Mechanisms-An Updated Review.
Review in NeuroSci, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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
17 citing papers in PubMed.
- Tissue engineering for traumatic spinal cord injury: Research advances and clinical translation.Bioactive materials · 2026Review
- Trehalose's untapped mechanisms in alzheimer's: gut-brain-autophagy signalling beyond the usual targets.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026Review
- Autophagy at the Crossroads of Protein and RNA Toxicity in Repeat Expansion Cerebellar Ataxias.Cells · 2026Review
- Substrate-Driven Modulation of Nutritional Composition and Bioactive Compound Profile inFoods (Basel, Switzerland) · 2026Article
- Exercise-Driven NRF2 Activation as a Systemic Neuroprotective Strategy: Integrating Redox Biology, Muscle-Brain Crosstalk, and Therapeutic Targeting in Neurodegeneration.Biochemical genetics · 2026Review
- Aminochrome-Induced Disruption of Autophagosome-Lysosome Fusion: Implications for Protein Aggregation in Parkinson's Disease.Antioxidants (Basel, Switzerland) · 2026Article
- Deletion of low-essentiality, secretion-associated genes enhances recombinant protein production in Komagataella phaffii.Microbial cell factories · 2026Article
- Anhydrobiosis as a Model of Aging and Longevity: The Role of Autophagy and Metabolism in Yeast Cells.Microbial ecology · 2026Review
- From heat stress to recovery: proteomic insights into endangered Brachymystax tsinlingensis survival strategies and the ameliorative effects of anti-stress additives.Stress biology · 2025Article
- Trehalose enhances neuronal differentiation with VEGF secretion in human iPSC-derived neural stem/progenitor cells.Regenerative therapy · 2025Article
- Polyphenol-Loaded Nanodevices as Innovative Therapeutic Strategies for Dry Eye Disease: Advances and Perspectives.Antioxidants (Basel, Switzerland) · 2025Review
- Review
- Cellular Models of Aging and Senescence.Cells · 2025Review
- Autophagy and Its Association with Macrophages in Clonal Hematopoiesis Leading to Atherosclerosis.International journal of molecular sciences · 2025Review
- Trehalose Ameliorates Zebrafish Emotional and Social Deficits Caused by CLN8 Dysfunction.Cells · 2025Article
- Nutritional strategies against dementia in rural populations.Frontiers in nutrition · 2025Review
- Dietary Trehalose Activates Autophagy Potentially Via MAPK Signaling Pathway to Alleviate Oxidative Stress Induced by Air Exposure Stress in Chinese Mitten Crab (Aquaculture nutrition · 2025Article
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Trehalose is a naturally occurring disaccharide that has recently gained significant attention for its neuroprotective properties in various models of neurodegeneration. This review provides an overview of available experimental data on the beneficial properties of trehalose for central nervous system pathological conditions. Trehalose's impact on neuronal cell survival and function was also examined. As a result, we identified that trehalose's neuroprotection includes autophagy modulation as well as its capability to stabilize proteins and inhibit the formation of misfolded ones. Moreover, trehalose mitigates oxidative stress-induced neuronal damage by stabilizing cellular membranes and modulating mitochondrial function. Furthermore, trehalose attenuates excitotoxicity-induced neuroinflammation by suppressing pro-inflammatory cytokine release and inhibiting inflammasome activation. A possible connection of trehalose with the gut-brain axis was also examined. These findings highlight the potential therapeutic effects of trehalose in neurodegenerative diseases. According to the conclusions drawn from this study, trehalose is a promising neuroprotective agent as a result of its distinct mechanism of action, which makes this compound a candidate for further research and the development of therapeutic strategies to combat neuronal damage and promote neuroprotection in various neurological diseases.
Indexed as
Identifiers
What Socratic 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 Socratic graph.