Signaling pathway cross talk in Alzheimer's disease

Juan A. Godoy, Juvenal A. Rios, Juan M. Zolezzi, Nady Braidy, Nibaldo C. Inestrosa*

*Corresponding author for this work

Research output: Contribution to journalArticle

86 Citations (Scopus)
23 Downloads (Pure)

Abstract

Numerous studies suggest energy failure and accumulative intracellular waste play a causal role in the pathogenesis of several neurodegenerative disorders and Alzheimer's disease (AD) in particular. AD is characterized by extracellular amyloid deposits, intracellular neurofibrillary tangles, cholinergic deficits, synaptic loss, inflammation and extensive oxidative stress. These pathobiological changes are accompanied by significant behavioral, motor, and cognitive impairment leading to accelerated mortality. Currently, the potential role of several metabolic pathways associated with AD, including Wnt signaling, 5' adenosine monophosphate-activated protein kinase (AMPK), mammalian target of rapamycin (mTOR), Sirtuin 1 (Sirt1, silent mating-type information regulator 2 homolog 1), and peroxisome proliferator-activated receptor gamma co-activator 1-α (PGC-1α) have widened, with recent discoveries that they are able to modulate several pathological events in AD. These include reduction of amyloid-β aggregation and inflammation, regulation of mitochondrial dynamics, and increased availability of neuronal energy. This review aims to highlight the involvement of these new set of signaling pathways, which we have collectively termed "anti-ageing pathways", for their potentiality in multi-target therapies against AD where cellular metabolic processes are severely impaired.

Original languageEnglish
Article number23
Pages (from-to)1-12
Number of pages12
JournalCell Communication and Signaling
Volume12
Issue number1
DOIs
Publication statusPublished - 28 Mar 2014
Externally publishedYes

Bibliographical note

Copyright the Author(s) 2014. Version archived for private and non-commercial use with the permission of the author/s and according to publisher conditions. For further rights please contact the publisher.

Keywords

  • Alzheimer's disease
  • Cognitive decline
  • Neurodegeneration
  • Neuronal network failure
  • Reactive oxygen species

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