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Related Concept Videos

Autism Spectrum Disorder01:19

Autism Spectrum Disorder

Autism spectrum disorder (ASD) is a neurodevelopmental condition marked by persistent deficits in social communication and interaction alongside restrictive and repetitive behaviors or interests. ASD is sometimes accompanied by intellectual impairment.
These core symptoms manifest differently among individuals, ranging from mild to severe. The disorder's complexity extends beyond its clinical presentation, encompassing a diverse range of biological, cognitive, and sociocultural influences.
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Alzheimer Disease ll: Pathophysiology

Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and microglia. Abnormal...
Biological Causes of Schizophrenia01:29

Biological Causes of Schizophrenia

Schizophrenia, a severe psychiatric disorder, arises from a complex interplay of biological factors, including genetic predisposition, structural brain abnormalities, neurotransmitter dysregulation, and developmental irregularities. These factors collectively contribute to the onset and progression of the disorder, which typically manifests in late adolescence or early adulthood.
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Disorders of the Nervous Tissue01:28

Disorders of the Nervous Tissue

Nervous tissue is a vital component of the human body's communication system, enabling us to perceive and respond to stimuli. However, like all other tissues, it is vulnerable to disorders and diseases that can significantly impact our neurological functioning.
Homeostatic Imbalances:
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Long-term Depression01:03

Long-term Depression

Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
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Related Experiment Video

Updated: May 23, 2026

Dynamic Clamp Methods to Investigate Impaired Neuronal Excitability Associated with Autism
08:44

Dynamic Clamp Methods to Investigate Impaired Neuronal Excitability Associated with Autism

Published on: October 17, 2025

Cellular and synaptic network defects in autism.

João Peça1, Guoping Feng

  • 1McGovern Institute for Brain Research, Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.

Current Opinion in Neurobiology
|March 24, 2012
PubMed
Summary
This summary is machine-generated.

Genetic links between autism spectrum disorders (ASDs) and specific syndromes like Tuberous Sclerosis Complex are emerging. Understanding synaptic gene interactions is key to unraveling ASD complexity.

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Area of Science:

  • Neuroscience
  • Genetics
  • Molecular Biology

Background:

  • Autism spectrum disorders (ASDs) are complex neurodevelopmental conditions with numerous candidate susceptibility genes.
  • These genes often converge on common cellular pathways, particularly those involved in synaptic function.
  • Several specific genetic syndromes share overlapping genetic links with ASDs.

Purpose of the Study:

  • To review interrelated gene complexes associated with ASD susceptibility.
  • To explore the common organizational principles of glutamatergic synapses.
  • To propose a link between genes implicated in Tuberous Sclerosis Complex, Fragile X syndrome, Angelman syndrome, and synaptic ASD candidate genes.

Main Methods:

  • Literature review of genetic studies and pathway analyses related to ASDs.
  • Examination of gene families and their functional convergence on cellular pathways.
  • Integration of knowledge on synaptic organization and dysfunction in neural networks.

Main Results:

  • Identification of four interrelated gene complexes functionally coalescing on common cellular pathways relevant to ASDs.
  • Illustration of a common organizational theme in glutamatergic synapse development and function.
  • A suggested link between genes involved in specific neurodevelopmental syndromes and synaptic ASD candidate genes.

Conclusions:

  • Understanding the molecular architecture of protein-protein interactions is crucial for ASD research.
  • Investigating synaptic dysfunction in neural networks offers insights into ASD pathogenesis.
  • A systems-level approach integrating genetic and synaptic data may advance ASD understanding.