Cell cultures from animal models of Alzheimer's disease as a tool for faster screening and testing of drug efficacy

J Mol Neurosci. 2004;24(1):15-21. doi: 10.1385/JMN:24:1:015.

Abstract

Approximately 2 million people in the United States suffer from Alzheimer's disease (AD), which is the most common cause of chronic dementia among the aging population. During the last 7 yr, excellent opportunities to screen drugs against AD have been provided by animal models of the disease. Because even in the fastest model, AD pathology does not start before the end of the second month, it has been necessary to wait at least until that age to inject drugs into the animal to assess whether they prevent, reduce, or revert synaptic impairment, plaque formation, and increase of beta-amyloid (Abeta) levels, the main features of the disease. A solution to the problems mentioned above is achieved by the present fast, efficient, and reproducible cultured cell system from animal models of AD or Abeta-associated diseases, for the screening and testing of compounds for the treatment and therapy of AD or Abeta-associated diseases.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Age Factors
  • Alzheimer Disease / drug therapy*
  • Alzheimer Disease / genetics
  • Alzheimer Disease / metabolism
  • Amyloid beta-Peptides / antagonists & inhibitors
  • Amyloid beta-Peptides / metabolism
  • Amyloid beta-Protein Precursor / genetics
  • Amyloid beta-Protein Precursor / metabolism
  • Animals
  • Cell Culture Techniques / methods
  • Cells, Cultured
  • Disease Models, Animal
  • Drug Evaluation, Preclinical / methods*
  • Drug Evaluation, Preclinical / trends
  • Excitatory Postsynaptic Potentials / drug effects
  • Excitatory Postsynaptic Potentials / physiology
  • Glutamic Acid / metabolism
  • Glutamic Acid / pharmacology
  • Hippocampus / drug effects
  • Hippocampus / metabolism
  • Hippocampus / physiopathology
  • Humans
  • Membrane Proteins / genetics
  • Membrane Proteins / metabolism
  • Mice
  • Mice, Transgenic
  • Neuronal Plasticity / drug effects
  • Neuronal Plasticity / genetics
  • Neuroprotective Agents / pharmacology*
  • Presenilin-1
  • Presynaptic Terminals / drug effects
  • Presynaptic Terminals / metabolism
  • Synapsins / drug effects
  • Synapsins / metabolism
  • Time Factors
  • Treatment Outcome
  • Up-Regulation / drug effects
  • Up-Regulation / physiology

Substances

  • Amyloid beta-Peptides
  • Amyloid beta-Protein Precursor
  • Membrane Proteins
  • Neuroprotective Agents
  • PSEN1 protein, human
  • Presenilin-1
  • Synapsins
  • Glutamic Acid