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Intracerebroventricular Injection of Amyloid-β Peptides in Normal Mice to Acutely Induce Alzheimer-like Cognitive Deficits
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Anti-aβ therapeutics in Alzheimer's disease: the need for a paradigm shift

Todd E Golde1, Lon S Schneider, Edward H Koo

  • 1Center for Translational Research in Neurodegenerative Disease and Department of Neuroscience, College of Medicine, University of Florida, 1275 Center Drive BMS J-483, P.O. Box 100159, Gainesville, FL 32610-0244, USA. tgolde@mbi.ufl.edu

Neuron
|January 26, 2011
PubMed

Insights

Current Alzheimer's disease (AD) treatments targeting amyloid beta-peptide (Aβ) may be ineffective in symptomatic patients. Resolving the treatment versus prevention dilemma is crucial for developing effective AD therapeutics.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Biomedical Research

Background:

  • Alzheimer's disease (AD) therapies in development primarily target amyloid beta-peptide (Aβ) production, aggregation, or accumulation.
  • Translational models indicate that anti-Aβ therapies could be most effective when used for disease prevention or in asymptomatic individuals with early AD pathology.

Purpose of the Study:

  • To highlight the critical treatment versus prevention dilemma in current Alzheimer's disease (AD) therapeutic development.
  • To discuss the misalignment between clinical studies and preclinical findings regarding anti-amyloid beta-peptide (Aβ) therapies.
  • To propose strategies for resolving this dilemma and advancing the development of effective AD treatments.

Main Methods:

  • This perspective reviews current trends in AD drug development.
  • It analyzes the implications of targeting amyloid beta-peptide (Aβ) at different disease stages.
  • It synthesizes insights from translational models and clinical trial observations.

Main Results:

  • Current anti-amyloid beta-peptide (Aβ) therapeutics are being tested in symptomatic Alzheimer's disease (AD) patients, where they are predicted to have limited efficacy.
  • A significant gap exists between the optimal timing suggested by preclinical models and the actual testing of these therapies in clinical trials.
  • The current approach creates a "treatment versus prevention" dilemma, potentially hindering therapeutic success.

Conclusions:

  • It is imperative to resolve the treatment versus prevention dilemma to enhance the development of effective Alzheimer's disease (AD) therapeutics.
  • Future strategies should consider targeting amyloid beta-peptide (Aβ) earlier in the disease process, aligning with preclinical evidence.
  • Moving forward requires a re-evaluation of clinical trial designs for anti-Aβ agents to improve their potential for success in combating AD.

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