Abstract
Despite the great number of observations being made concerning cellular and the molecular dysfunctions associated with autism spectrum disorders (ASD), the basic central mechanism of these disorders has not been proposed in the major scientific literature. Our review brings evidence that most heterogeneous symptoms of ASD have a common set of events closely connected with dysregulation of glutamatergic neurotransmission in the brain with enhancement of excitatory receptor function by pro-inflammatory immune cytokines as the underlying mechanism. We suggest that environmental and dietary excitotoxins, mercury, fluoride, and aluminum can exacerbate the pathological and clinical problems by worsening excitotoxicity and by microglial priming. In addition, each has effects on cell signaling that can affect neurodevelopment and neuronal function. Our hypothesis opens the door to a number of new treatment modes, including the nutritional factors that naturally reduce excitotoxicity and brain inflammation.
Keywords: Autism spectrum disorders, excitotoxicity, fluoride, glutamatergic neurotransmission, inflammation, mercury, microglia, cytokines
Current Medicinal Chemistry
Title: Immune-Glutamatergic Dysfunction as a Central Mechanism of the Autism Spectrum Disorders
Volume: 16 Issue: 2
Author(s): R. L. Blaylock and A. Strunecka
Affiliation:
Keywords: Autism spectrum disorders, excitotoxicity, fluoride, glutamatergic neurotransmission, inflammation, mercury, microglia, cytokines
Abstract: Despite the great number of observations being made concerning cellular and the molecular dysfunctions associated with autism spectrum disorders (ASD), the basic central mechanism of these disorders has not been proposed in the major scientific literature. Our review brings evidence that most heterogeneous symptoms of ASD have a common set of events closely connected with dysregulation of glutamatergic neurotransmission in the brain with enhancement of excitatory receptor function by pro-inflammatory immune cytokines as the underlying mechanism. We suggest that environmental and dietary excitotoxins, mercury, fluoride, and aluminum can exacerbate the pathological and clinical problems by worsening excitotoxicity and by microglial priming. In addition, each has effects on cell signaling that can affect neurodevelopment and neuronal function. Our hypothesis opens the door to a number of new treatment modes, including the nutritional factors that naturally reduce excitotoxicity and brain inflammation.
Export Options
About this article
Cite this article as:
Blaylock L. R. and Strunecka A., Immune-Glutamatergic Dysfunction as a Central Mechanism of the Autism Spectrum Disorders, Current Medicinal Chemistry 2009; 16(2) . https://dx.doi.org/10.2174/092986709787002745
DOI https://dx.doi.org/10.2174/092986709787002745 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |

- Author Guidelines
- Graphical Abstracts
- Fabricating and Stating False Information
- Research Misconduct
- Post Publication Discussions and Corrections
- Publishing Ethics and Rectitude
- Increase Visibility of Your Article
- Archiving Policies
- Peer Review Workflow
- Order Your Article Before Print
- Promote Your Article
- Manuscript Transfer Facility
- Editorial Policies
- Allegations from Whistleblowers
- Announcements
- Forthcoming Thematic Issues
Related Articles
-
Gold - Old Drug with New Potentials
Current Medicinal Chemistry 2, 5-Disubstituted Phthalimides: Design, Synthesis and Anticonvulsant Activity in scPTZ and MES Models
Current Computer-Aided Drug Design Mitochondrial Dysfunction and Targeted Drugs: A Focus on Diabetes
Current Pharmaceutical Design Acid-Sensing Ion Channels Structural Aspects, Pathophysiological Importance and Experimental Mutational Data Available Across Various Species to Target Human ASIC1
Current Drug Targets Future Directions for Pharmacotherapies for Treatment-resistant Bipolar Disorder
Current Neuropharmacology Biological Evaluation of Imidazobenzoxazines, Imidazobenzoxazin-5-ones and Imidazobenzoxazin-5-thiones as Sodium Channel Blockers
Letters in Drug Design & Discovery Extracellular Vesicles in Glioblastoma: Role in Biological Processes and in Therapeutic Applications
Current Cancer Drug Targets Therapeutic Strategies for Treatment of Inflammation-related Depression
Current Neuropharmacology Analysis of Functional Brain Images Using Population-Based Probabilistic Atlas
Current Medical Imaging Poor Safety and Tolerability Hamper Reaching a Potentially Therapeutic Dose in the Use of Thalidomide for Alzheimer’s Disease: Results from a Double-Blind, Placebo-Controlled Trial
Current Alzheimer Research The Influence of Genetic Variations and Drug Interactions Based on Metabolism of Antidepressants and Anticonvulsants
Current Drug Metabolism Role of Methylene Blue in Trauma Neuroprotection and Neuropsychiatric Diseases
CNS & Neurological Disorders - Drug Targets Calcium Channels and Prostate Cancer
Recent Patents on Anti-Cancer Drug Discovery Menthone Aryl Acid Hydrazones: A New Class of Anticonvulsants
Medicinal Chemistry AMPA Receptor Antagonists with Additional Mechanisms of Action: New Opportunities for Neuroprotective Drugs?
Current Pharmaceutical Design Neuroprotective Effects of Exercise Treatments After Injury: The Dual Role of Neurotrophic Factors
Current Neuropharmacology Genetic Polymorphism of Organic Anion and Cation Transporters: Pharmacokinetic and Pharmacodynamic Consequences in Pharmacotherapy
Current Pharmacogenomics Nitric Oxide and Teratogenesis: An Update
Current Pharmaceutical Design The Effect of Mianserin on Lifespan of <i>Caenorhabditis elegan</i> is Abolished by Glucose
Current Aging Science Pharmacology of Recombinant Low-Voltage Activated Calcium Channels
Current Drug Targets - CNS & Neurological Disorders