A novel perspective on tau in alzheimer's disease

D. J. Bonda, R. J. Castellani, X. Zhu, A. Nunomura, H. G. Lee, G. Perry*, M. A. Smith

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

26 Scopus citations


Mainstream thinking is dominated by the notion that the aggregation of specific proteins within neurons, and their subsequent formation into cytoplasmic and extracellular lesions, directly elicits neuronal dysfunction and death. Current dogma, for example, maintains that phosphorylated tau protein, the major component of neurofibrillary tangles, is a central mediator of disease pathogenesis. In this article, we challenge this classic notion by proposing that tau phosphorylation represents a compensatory response mounted by neurons against oxidative stress that serves a protective function. This concept provides a better understanding of the mechanisms underlying disease pathophysiology and also provides a window for therapeutic intervention.

Original languageEnglish (US)
Pages (from-to)639-642
Number of pages4
JournalCurrent Alzheimer Research
Issue number6
StatePublished - Sep 2011


  • Alzheimer disease
  • Neuron
  • Oxidative stress
  • Phosphorylation
  • Tau

ASJC Scopus subject areas

  • Clinical Neurology
  • Neurology


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