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Related Concept Videos

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...
Amyloid Fibrils03:03

Amyloid Fibrils

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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Amyloid Fibrils03:03

Amyloid Fibrils

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, normally used to...
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...
Alzheimer Disease l: Introduction01:29

Alzheimer Disease l: Introduction

Alzheimer disease is a chronic, progressive, and irreversible neurodegenerative disorder and the most common cause of dementia in older adults. It leads to gradual neuronal loss, causing cognitive decline, behavioral changes, and loss of functional independence.Risk Factors and EtiologyThe disease is multifactorial. Age is the strongest risk factor, with prevalence doubling every 5 years after age 65. Genetic factors include mutations in genes such as APP, PSEN1, and PSEN2, which are associated...

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Visualization of Amyloid β Deposits in the Human Brain with Matrix-assisted Laser Desorption/Ionization Imaging Mass Spectrometry
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Changes in readthrough acetylcholinesterase expression modulate amyloid-beta pathology.

Amit Berson1, Marlen Knobloch, Mor Hanan

  • 1The Eric Roland Center for Neurodegenerative Diseases, Institute of Life Sciences, The Hebrew University of Jerusalem, 91904 Jerusalem, Israel.

Brain : a Journal of Neurology
|December 7, 2007
PubMed
Summary

Alzheimer's disease involves cholinergic deficits. The AChE-R variant protects against amyloid beta toxicity, unlike AChE-S, suggesting its loss exacerbates Alzheimer's pathology.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Alzheimer's disease (AD) is linked to cholinergic deficits.
  • The role of acetylcholinesterase (AChE) splice variants in AD amyloid pathology is unclear.
  • Synaptic AChE (AChE-S) accelerates amyloid-beta (Abeta) fibril formation.

Purpose of the Study:

  • Investigate the neuroprotective potential of the AChE-R splice variant against Abeta toxicity.
  • Clarify the opposing roles of AChE-S and AChE-R in AD pathogenesis.
  • Examine the expression and protein levels of AChE variants in AD patient brains.

Main Methods:

  • In vitro studies using purified AChE-R to assess Abeta aggregation and cell toxicity.
  • In vivo studies using APPsw/AChE-R double transgenic mice.
  • Analysis of hippocampal tissue from AD patients (n=10) for mRNA and protein levels of AChE variants.

Main Results:

  • AChE-R dose-dependently suppressed insoluble Abeta oligomer/fibril formation and abolished Abeta-induced cell toxicity in vitro.
  • APPsw/AChE-R mice exhibited reduced plaque burden, fewer reactive astrocytes, and less dendritic damage compared to APPsw mice.
  • AD patient hippocampi showed elevated AChE-R mRNA but drastically reduced intact AChE-R protein levels, with reduced AChE-S mRNA.

Conclusions:

  • The AChE-R splice variant exerts neuroprotective effects against Abeta toxicity, opposing AChE-S.
  • Selective loss of functional AChE-R protein in AD brains may exacerbate Abeta-induced damage.
  • A previously unrecognized link exists between cholinergic gene expression and amyloid pathology in Alzheimer's disease.