Molecular neuropathogenesis of Alzheimers disease: An interaction model stressing the central role of oxidative stress

Roberto Rodrigues, Mark A. Smith, Xinglong Wang, George Perry, Hyoung Gon Lee, Xiongwei Zhu, Robert B. Petersen

Research output: Contribution to journalReview articlepeer-review

13 Scopus citations

Abstract

Alzheimers disease (AD) exhibits a complex etiology that simultaneously manifests as a complex cellular, neurobiological, molecular, anatomic-physiological and clinical entity. Other significant psychiatric conditions, such as depression and schizophrenia, may also present with complex and concurrent clinical and/or molecular phenotypes. These neuropsychiatric pathologies also originate from both environmental and genetic factors. We analyzed the molecular phenotypes of AD and discuss them with respect to the classical theories, which we integrated into mechanisms that share molecular and/or anatomical connections. Based on these mechanisms, we propose an interaction model and discuss the model in light of studies that refute or support it. Given the spectrum of AD phenotypes, we limit the scope of our discussion to a few, which facilitates concrete analysis. In addition, the study of specific, individual pathogenic phenotypes may be critical to defining the complex mechanisms leading to AD, thereby improving strategies for developing novel therapies.

Original languageEnglish (US)
Pages (from-to)287-305
Number of pages19
JournalFuture Neurology
Volume7
Issue number3
DOIs
StatePublished - May 2012
Externally publishedYes

Keywords

  • Alzheimer's disease
  • amyloid-b
  • apolipoprotein E
  • neurofibrillary tangles
  • Parkinson's disease
  • reactive oxygen species

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

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