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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...
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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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Related Experiment Video

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Neurodegeneration in an Animal Model of Chronic Amyloid-beta Oligomer Infusion Is Counteracted by Antibody Treatment Infused with Osmotic Pumps
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Neuroprotective natural antibodies to assemblies of amyloidogenic peptides decrease with normal aging and advancing

M Britschgi1, C E Olin, H T Johns

  • 1Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA.

Proceedings of the National Academy of Sciences of the United States of America
|July 8, 2009
PubMed
Summary

Natural antibodies targeting toxic beta-amyloid (Abeta) species decline with age and Alzheimer's disease (AD). These antibodies, found in humans and primates, show protective effects against Abeta toxicity, suggesting a potential preventive strategy for AD.

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Published on: July 14, 2010

Area of Science:

  • Neuroscience
  • Immunology
  • Biochemistry

Background:

  • Alzheimer's disease (AD) is linked to various beta-amyloid (Abeta) forms.
  • Natural human antibodies against Abeta exist, but their population-level characteristics are poorly understood.
  • Current AD therapies include antibodies targeting Abeta peptides.

Purpose of the Study:

  • To investigate the presence, diversity, and function of natural antibodies against Abeta and related amyloidogenic peptides in humans and non-human primates.
  • To determine how antibody reactivity against Abeta species changes with age and AD progression.
  • To assess the neuroprotective potential of naturally occurring and induced antibodies against Abeta toxicity.

Main Methods:

  • Peptide microarrays were used to screen plasma and cerebrospinal fluid from AD patients and healthy controls.
  • Antibody reactivity was analyzed against various Abeta species, including oligomeric, pyroglutamate, and oxidized forms.
  • IgG isolation and in vitro assays were performed to evaluate the neuroprotective effects of antibodies.
  • Aged vervet monkeys were used to study natural antibody patterns and immune responses after Abeta immunization.

Main Results:

  • Natural antibodies against toxic Abeta and non-Abeta amyloid species were detected in human plasma and cerebrospinal fluid across a wide age range.
  • Antibody reactivity was highest against oligomeric Abeta and modified residues; IgG levels specific for oligomeric Abeta1-42 decreased with age and AD.
  • Antibodies from both AD patients and healthy controls demonstrated neuroprotective capabilities against Abeta toxicity in vitro.
  • Vervet monkeys exhibited similar antibody patterns to humans and developed cross-reactive antibodies against mutant Abeta peptides after immunization.

Conclusions:

  • Conformation-specific, cross-reactive antibodies may offer protection against toxic amyloidogenic peptides.
  • Declining natural antibody levels with age and AD suggest a potential role in disease pathogenesis.
  • Harnessing these natural antibodies, either by stimulation or passive administration, could represent a novel preventive strategy for Alzheimer's disease.