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Related Concept Videos

Alzheimer's Disease: Treatment01:22

Alzheimer's Disease: Treatment

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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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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. 
Amyloid deposits were observed as early as 1639 in the liver and the spleen.   In 1854, Rudolph Virchow performed iodine staining,...
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Reduction of Amyloid-β Production without Inhibiting Secretase Activity by MS-275.

Yachiyo Mitsuishi1, Masaki Nakano1, Hirotatsu Kojima2

  • 1Molecular Neuroscience Research Center, Shiga University of Medical Science, Shiga 520-2192, Japan.

ACS Chemical Neuroscience
|February 28, 2024
PubMed
Summary
This summary is machine-generated.

MS-275, a histone deacetylase inhibitor, reduces amyloid-beta (Aβ) production in Alzheimer's disease models by mimicking ILEI activity. This compound offers a potential therapeutic strategy for lowering brain Aβ accumulation without inhibiting secretase activity.

Keywords:
Alzheimer’s diseaseAβ productionbrain amyloid-βchronic MS-275 treatmenthistone deacetylasesinterleukin-like epithelial-to-mesenchymal transition inducer

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pharmacology

Background:

  • Brain amyloid-beta (Aβ) is central to Alzheimer's disease pathogenesis.
  • Previous therapeutic strategies targeting β- and γ-secretases have yielded limited clinical benefit and adverse events.
  • Interleukin-like epithelial-to-mesenchymal transition inducer (ILEI) reduces Aβ production independently of secretase inhibition.

Purpose of the Study:

  • To investigate the potential of MS-275, a histone deacetylase (HDAC) inhibitor, to reduce Aβ production.
  • To determine if MS-275's Aβ-lowering effects are linked to HDAC inhibition or mimic ILEI activity.
  • To evaluate the efficacy of chronic MS-275 treatment in an Alzheimer's disease mouse model.

Main Methods:

  • Assessed the effect of MS-275 on Aβ production.
  • Investigated the mechanism of MS-275, specifically its relation to HDAC inhibition and ILEI-like activity.
  • Administered chronic MS-275 treatment to an Alzheimer's disease mouse model.

Main Results:

  • MS-275 reduced Aβ production through an ILEI-like mechanism, independent of HDAC inhibition.
  • Chronic MS-275 treatment significantly decreased Aβ deposition in the cerebral cortex and hippocampus of the Alzheimer's disease mouse model.
  • MS-275 demonstrated efficacy in reducing brain Aβ accumulation.

Conclusions:

  • MS-275 exhibits therapeutic potential for Alzheimer's disease by reducing brain Aβ accumulation.
  • The compound acts via an ILEI-mimetic pathway, offering an alternative to secretase inhibition.
  • MS-275 represents a promising candidate for further development in Alzheimer's disease treatment.