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Related Concept Videos

Alzheimer's Disease: Treatment01:22

Alzheimer's Disease: Treatment

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...
Alzheimer Disease ll: Pathophysiology01:23

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...
The Proteasome01:13

The Proteasome

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.
In this pathway, the target proteins are first tagged with small proteins called ubiquitin. This involves participation of a series of enzymes including— E1 (ubiquitin-activating enzyme), E2 (ubiquitin-conjugating enzyme), and E3 (ubiquitin...
The Proteasome02:18

The Proteasome

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.
In this pathway, the target proteins are first tagged with small proteins called ubiquitin. A series of enzymes carry out the ubiquitination of the target proteins - E1 (ubiquitin-activating enzyme), E2 (ubiquitin-conjugating enzyme), and E3...
Alzheimer's Disease: Overview01:26

Alzheimer's Disease: Overview

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.
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ and tau...
Covalently Linked Protein Regulators02:04

Covalently Linked Protein Regulators

Proteins can undergo many types of post-translational modifications, often in response to changes in their environment. These modifications play an important role in the function and stability of these proteins. Covalently linked molecules include functional groups, such as methyl, acetyl, and phosphate groups, and also small proteins, such as ubiquitin. There are around 200 different types of covalent regulators that have been identified.
These groups modify specific amino acids in a protein.

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Updated: May 28, 2026

Characterizing Histone Post-translational Modification Alterations in Yeast Neurodegenerative Proteinopathy Models
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Published on: March 24, 2019

Protein Modifications and Quality Control System: Target for Alzheimer's Disease Therapy.

Abdullah Md Sheikh1, Shozo Yano1,2, Shatera Tabassum3

  • 1Department of Laboratory Medicine, Faculty of Medicine, Shimane University, 89-1 Enya Cho, Izumo 693-8501, Japan.

International Journal of Molecular Sciences
|May 27, 2026
PubMed
Summary
This summary is machine-generated.

Alzheimer's disease involves complex protein issues beyond amyloid-beta (Aβ) plaques. Targeting post-translational modifications (PTMs) and protein quality control (PQC) offers new therapeutic avenues for neurodegenerative disorders.

Keywords:
Alzheimer’s diseaseamyloid β peptideneurodegenerationneuroinflammationsposttranslational modificationprotein quality control systemtau

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Published on: March 24, 2019

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Area of Science:

  • Neuroscience
  • Biochemistry
  • Pathology

Background:

  • Alzheimer's disease (AD) is a progressive neurodegenerative disorder marked by memory loss and cognitive decline.
  • Key pathologies include amyloid-beta (Aβ) plaques and hyperphosphorylated tau tangles.
  • Current Aβ-targeting therapies show limited clinical efficacy, suggesting complex disease mechanisms.

Purpose of the Study:

  • To explore the role of post-translational modifications (PTMs) and protein quality control (PQC) in Alzheimer's disease pathogenesis.
  • To investigate how PTMs and PQC dysfunction contribute to Aβ and tau pathology.
  • To propose novel therapeutic strategies targeting PTMs and PQC for AD.

Main Methods:

  • Review of existing literature on PTMs (phosphorylation, ubiquitination, acetylation, glycosylation, oxidation) of Aβ and tau.
  • Analysis of the role of protein quality control (PQC) systems in maintaining proteostasis in AD.
  • Synthesis of evidence linking PTM dysregulation and PQC impairment to AD progression.

Main Results:

  • PTMs significantly influence the structure, aggregation, and toxicity of Aβ and tau.
  • Impaired PQC systems lead to inefficient clearance of abnormal proteins in AD.
  • Dysfunctional PTMs and PQC act convergently to drive AD pathogenesis.

Conclusions:

  • Alzheimer's disease pathogenesis is driven by a complex interplay of PTMs and PQC dysfunction, not solely Aβ accumulation.
  • Targeting PTMs and PQC offers a promising strategy for developing more effective AD therapies.
  • This approach may lead to sustained disease modification beyond current Aβ-centric treatments.