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Related Concept Videos

Alzheimer's Disease: Treatment01:22

Alzheimer's Disease: Treatment

161
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 Fibrils03:03

Amyloid Fibrils

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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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Alzheimer's Disease: Overview01:26

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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.
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ...
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Related Experiment Video

Updated: Jun 2, 2025

A11-positive &#946;-amyloid Oligomer Preparation and Assessment Using Dot Blotting Analysis
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The Missing Link in Antiamyloid Therapy.

Pravat K Mandal1,2, Joseph C Maroon1, Rimil Guha Roy3

  • 1Department of Neurological Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania 15213, United States.

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|January 15, 2025
PubMed
Summary
This summary is machine-generated.

Alzheimer's disease may be linked to oxidative stress and glutathione depletion. A new approach combines lecanemab with glutathione precursor gamma-glutamylcysteine to potentially improve outcomes.

Keywords:
Alzheimer’s diseaseantiamyloid drugsantioxidantscognitive reservecombinational therapyglutathionelecanemaboxidative stress

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Selection of Aptamers for Amyloid &#946;-Protein, the Causative Agent of Alzheimer's Disease
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Selection of Aptamers for Amyloid &#946;-Protein, the Causative Agent of Alzheimer's Disease
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Area of Science:

  • Neuroscience
  • Biochemistry
  • Gerontology

Background:

  • Alzheimer's disease (AD) causes significant cognitive decline in millions globally.
  • Current AD research and trials heavily focus on beta-amyloid and tau hypotheses.
  • Lecanemab showed modest cognitive delay but had significant adverse events like brain swelling and hemorrhages.

Purpose of the Study:

  • To explore the oxidative stress (OS) hypothesis in AD pathogenesis.
  • To investigate the role of glutathione (GSH) depletion in AD and mild cognitive impairment (MCI).
  • To propose a novel combination therapy for AD.

Main Methods:

  • Utilized magnetic resonance spectroscopy (MRS) to non-invasively measure brain GSH levels.
  • Correlated hippocampal GSH levels with memory impairment.
  • Proposed a therapeutic strategy combining lecanemab with oral gamma-glutamylcysteine (GGC).

Main Results:

  • Confirmed significant GSH depletion in the hippocampus of MCI and AD patients.
  • Observed a positive correlation between hippocampal GSH depletion and memory deficits.
  • Identified lecanemab's specificity for toxic protofibrils and beta-amyloid clearance.

Conclusions:

  • Oxidative stress and GSH depletion are likely early events in AD progression.
  • Combining lecanemab with GSH replenishment via GGC may offer a more effective therapeutic strategy.
  • This approach aims to mitigate adverse events and enhance clinical outcomes in AD treatment.