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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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Synaptic Function and Dysfunction in Lysosomal Storage Diseases.

Rima Rebiai1, Maria I Givogri1, Swetha Gowrishankar1

  • 1Department of Anatomy and Cell Biology, College of Medicine, The University of Illinois at Chicago, Chicago, IL, United States.

Frontiers in Cellular Neuroscience
|March 22, 2021
PubMed
Summary
This summary is machine-generated.

Lysosomal storage diseases (LSDs) cause neurological issues due to substrate buildup, affecting brain cells. This review explores how LSDs impair synaptic function, leading to cognitive decline.

Keywords:
GABALTDLTPcholesterolglutamate receptorslysosomessphingolipidssynapses

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Area of Science:

  • Neuroscience
  • Genetics
  • Metabolic disorders

Background:

  • Lysosomal storage diseases (LSDs) are inherited metabolic disorders.
  • Neurological involvement in LSDs leads to glial and neuronal dysfunction.
  • Accumulation of undegraded substrates damages gray and white matter, causing irreversible neuronal decline.

Purpose of the Study:

  • To discuss potential mechanisms of synaptic dysfunction in LSDs.
  • To explore how lysosomal dysfunction impacts neuronal function in LSDs.
  • To review findings from animal models regarding synaptic alterations in LSDs.

Main Methods:

  • Review of existing literature on LSDs and neurological dysfunction.
  • Analysis of mechanisms identified in animal models of LSDs.
  • Discussion of synaptic protein alterations, membrane structure, vesicle trafficking, and inflammation.

Main Results:

  • Animal models reveal synaptic protein deficits, altered membrane structure, and impaired vesicle dynamics.
  • Inflammation-mediated synaptic remodeling is implicated in LSD pathogenesis.
  • Mechanisms of cognitive deficits in LSDs remain largely unclear despite research.

Conclusions:

  • Synaptic dysfunction is a key factor in neurological manifestations of LSDs.
  • Further research is needed to fully elucidate pathogenetic mechanisms underlying cognitive deficits in LSDs.
  • Understanding these mechanisms is crucial for developing therapeutic strategies for LSDs.