Current strategies for the treatment of Alzheimer's disease and other tauopathies

Chad A. Dickey, Leonard Petrucelli

Research output: Contribution to journalArticle

21 Citations (Scopus)

Abstract

The pathological hallmarks of Alzheimer's disease (AD) include abnormal intra- and extraneuronal tau and amyloid accumulation, respectively, accompanied by gliosis, oxidative stress and neuron loss. The discovery of mutations within the tau gene itself that cause clinical dementia (i.e., fronto-temporal dementia with Parkinsonism linked to chromosome 17 [FrDP17]) demonstrated that disruption of normal tau function independent of amyloidogenesis was sufficient to cause neuronal loss and clinical dementia. These studies demonstrate the need for therapeutics that either decrease the total pool of tau or selectively reduce aberrant forms of tau (i.e., hyperphosphorylated, misfolded etc.). To this point, therapeutic development for tauopathies, including AD, have primarily focused on either the phosphorylation of tau, as it is a downstream target for many kinases and signalling cascades, or inhibition of tau aggregation. Recent developments, however, suggest that pharmacological targeting of other mechanisms may hold therapeutic promise for the treatment of tauopathies.

Original languageEnglish (US)
Pages (from-to)665-676
Number of pages12
JournalExpert Opinion on Therapeutic Targets
Volume10
Issue number5
DOIs
StatePublished - Oct 2006

Fingerprint

Tauopathies
Dementia
Alzheimer Disease
Phosphorylation
Oxidative stress
Chromosomes
Amyloid
Neurons
Chromosomes, Human, Pair 17
Gliosis
Phosphotransferases
Agglomeration
Genes
Parkinsonian Disorders
Oxidative Stress
Therapeutics
Pharmacology
Mutation

Keywords

  • Aggregation
  • Chaperone
  • Heat shock
  • Kinase
  • Phosphorylation
  • Tau

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Molecular Medicine

Cite this

Current strategies for the treatment of Alzheimer's disease and other tauopathies. / Dickey, Chad A.; Petrucelli, Leonard.

In: Expert Opinion on Therapeutic Targets, Vol. 10, No. 5, 10.2006, p. 665-676.

Research output: Contribution to journalArticle

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