Alzheimer's disease: Pathology vs etiology

Rudy J. Castellani, Hyoung Gon Lee, Xiongwei Zhu, Akihiko Nunomura, George Perry, Mark A. Smith

Research output: Contribution to journalReview articlepeer-review

Abstract

Evidence that amyloid-β is the etiological molecule in the pathogenesis of Alzheimer's disease (AD) is based on the edict that AD microscopic pathology contains a lesion or molecule without which neurodegeneration would not occur. This edict was the driving force behind the research that led to the discovery of amyloid-β, and continues to this day in the form of therapeutic trials targeting the microscopic pathology. If, on the other hand, the pathology represents an end-stage accumulation of proteins as physiological responses, the cascade that led to those accumulations would similarly represent an epiphenomenon. A logical appraisal of the pathology of AD as well as the consensus criteria for pathological diagnosis of AD, makes it manifestly clear that AD lesions are the result of the disease process, far removed from cause. The repeated modification and failure of lesion-directed therapies is thus empirical evidence that the amyloid cascade, although well characterised, is similarly a secondary process. The sooner the scientific and medical communities are able to reorganise their approach to AD pathogenesis, the better the disease will be understood overall in terms of cause and effect, and the more hope there will be for therapy that addresses early events.

Original languageEnglish (US)
Pages (from-to)36-40
Number of pages5
JournalInternational Journal of Neuroprotection and Neuroregeneration
Volume4
Issue number1
StatePublished - Oct 2007

Keywords

  • Alzheimer's disease
  • Amyloid-β
  • Etiology
  • Pathogenesis
  • Pathology

ASJC Scopus subject areas

  • Pharmacology
  • Clinical Neurology

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