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Related Concept Videos

The Proteasome01:13

The Proteasome

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Eukaryotic cells can degrade proteins through several pathways. One of the most important among these is the ubiquitin-proteasome pathway. It helps the cell eliminate the misfolded, damaged, or unwarranted cytoplasmic proteins in a highly specific manner.
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The Proteasome02:18

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Eukaryotic cells can degrade proteins through several pathways. One of the most important amongst these is the ubiquitin-proteasome pathway. It helps the cell eliminate the misfolded, damaged, or unwarranted cytoplasmic proteins in a highly specific manner.
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Role of Neurotransmitters in Memory01:23

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Neurotransmitters are integral to the brain's communication system, enabling neurons to transmit signals across synapses. This chemical exchange underpins various cognitive functions, including memory processes. The role of neurotransmitters in memory is multifaceted, influencing the encoding, consolidation, and retrieval of memories through their action on different neural circuits.
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Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
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Neurodegenerative disorders are progressive diseases that cause irreversible damage and loss to neurons in specific brain areas. Examples of these disorders include Parkinson's disease, Alzheimer's disease, Multiple Sclerosis (MS), and Amyotrophic Lateral Sclerosis (ALS). These disorders share characteristics such as proteinopathies, selective neuronal vulnerability, and a complex interplay between genetic and environmental factors. The primary therapeutic goal for these conditions is...
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Amyloid fibrils are aggregates of misfolded proteins.  Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils. 
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Quantifying Subcellular Ubiquitin-proteasome Activity in the Rodent Brain
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Decreased Proteasomal Function Induces Neuronal Loss and Memory Impairment.

Utano Tomaru1, Tomoki Ito1, Yu Ohmura2

  • 1Department of Pathology, Hokkaido University, Sapporo, Japan.

The American Journal of Pathology
|December 19, 2020
PubMed
Summary
This summary is machine-generated.

Age-related proteasome dysfunction impairs proteostasis, leading to Alzheimer disease (AD) hallmarks like memory loss and neuronal damage. This study links impaired proteasomal activity to endoplasmic reticulum stress, suggesting a key role in AD development.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Gerontology

Background:

  • Alzheimer disease (AD) is a major cause of dementia, with age-related proteostasis disruption implicated in its development.
  • The proteasome degrades proteins, and its age-related decline is linked to pathologies.
  • The exact role of proteasomal dysfunction in AD onset (causative vs. secondary) is unclear.

Purpose of the Study:

  • To investigate the causative role of proteasomal dysfunction in Alzheimer disease pathogenesis.
  • To explore the molecular mechanisms linking proteasomal dysfunction to neuronal damage and AD hallmarks.

Main Methods:

  • Utilized a mouse model with induced proteasomal dysfunction.
  • Examined neuronal loss, phosphorylated tau accumulation, and endoplasmic reticulum (ER) stress markers.
  • Investigated the effects of proteasomal inhibition in a murine hippocampal neuronal cell line (HT-22).
  • Tested the efficacy of a c-Jun N-terminal kinase inhibitor in preventing cell death.

Main Results:

  • Mice with proteasomal dysfunction showed memory impairment, neuronal loss, and phosphorylated tau accumulation.
  • Proteasomal dysfunction activated ER stress-related apoptosis pathways in both mice and HT-22 cells.
  • Inhibition of ER stress via c-Jun N-terminal kinase pathway blocked proteasome inhibitor-induced cell death in HT-22 cells.

Conclusions:

  • Impaired proteasomal activity disrupts proteostasis, triggering ER stress-mediated apoptosis and neuronal loss, key events in Alzheimer disease.
  • Age-related decline in proteasomal function may contribute significantly to the development and progression of AD in the elderly.