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Related Concept Videos

Caspases01:24

Caspases

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Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside...
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Alzheimer's Disease (AD), a neurodegenerative disorder, is pathologically identified by amyloid plaques and neurofibrillary tangles composed of tau protein. AD pharmacotherapy aims to manage cognitive symptoms, delay disease progression, and treat behavioral symptoms. The treatment is primarily symptomatic and palliative, with no definitive disease-modifying therapy available. Cholinesterase inhibitors, including donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne), are...
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Targeting Caspases 3/6 and Cathepsins L/B May Decrease Laminopathy-Induced Apoptosis in Alzheimer's Disease.

Auob Rustamzadeh1,2, Abbas Tafakhori3, Armin Ariaei4

  • 1Cellular and Molecular Research Center, Research Institute for Prevention of Non-Communicable Diseases, Department of Anatomical Sciences, School of Medicine, Qazvin University of Medical Sciences, Qazvin, Iran.

Journal of Alzheimer'S Disease : JAD
|August 9, 2024
PubMed
Summary

Laminopathy in Alzheimer's disease involves specific protein changes. Inhibiting caspase 6 and cathepsin L may reduce neuronal apoptosis, but further in vivo studies are needed.

Keywords:
Alzheimer’s diseaselaminopathymolecular dynamicstranscriptome

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pharmacology

Background:

  • Laminopathy is a key factor in Alzheimer's disease (AD) pathogenesis, contributing to neuronal cell death.
  • Understanding the molecular mechanisms of laminopathy is crucial for developing effective AD treatments.

Purpose of the Study:

  • To identify potential therapeutic targets by analyzing enzyme and protein expression in Alzheimer's disease.
  • To evaluate the efficacy of potential inhibitors for enzymes implicated in laminopathy.

Main Methods:

  • Analyzed mRNA expression of cathepsins, caspases, and lamins from AD datasets (GSE5281, GSE28146).
  • Utilized molecular docking and 10ns/100ns atomistic molecular dynamics (MD) simulations with Martini 3.
  • Investigated two selected ligands (PubChem id: 608841, ChEMBL id: 550872) for binding stability and energy.

Main Results:

  • Upregulation of caspase 6 and lamin A/C observed in AD hippocampus, contrasting with cathepsin B, lamin b2, and caspase 3.
  • Significant correlation found between cathepsin B, lamin A/C, and caspase 6 expression in AD patients.
  • MD simulations indicated varying binding stabilities for the two tested ligands, with one showing higher free binding energy and the other greater stability.

Conclusions:

  • Lamin A/C, cathepsins B/L, caspase 6, and lamin B2 are implicated in AD-related laminopathy and apoptosis.
  • Simultaneous inhibition of caspase 6 and cathepsin L presents a potential strategy to mitigate apoptosis.
  • Further in vivo validation is necessary to confirm these findings and therapeutic potential.