Drug Design and Discovery in Alzheimer’s Disease


Atta-ur-Rahman, Mohammad Iqbal Choudhary

DOI: 10.2174/97816080582281150101
eISBN: 978-1-60805-822-8, 2014
ISBN: 978-1-60805-823-5
ISSN: 1574-0889 (Print)
ISSN: 2212-1064 (Online)

Indexed in: Book Citation Index, Science Edition, BIOSIS Previews, Scopus, EMBASE, EBSCO, Ulrich's Periodicals Directory.

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Targeting the GSK3β/β-catenin Signaling to Treat Alzheimer´s Disease: Plausible or Utopic?

- Pp. 623-642 (20)

Fares Zeidán-Chuliá and José Cláudio Fonseca Moreira


Alzheimer´s disease (AD) is a neurodegenerative disorder characterized by progressive memory loss, cognitive impairment, and at the molecular level, by the presence of neurofibrillary tangles (NFTs). As opposed to degeneration, it is known that some specific regions of the brain contain neural stem cells (NSCs) able to produce neurons during adulthood. Wnt/β-catenin signaling has been described as a key pathway modulating the balance between NSC proliferation and differentiation. Wnt signaling is regulated by glycogen synthase kinase 3 (GSK3) that is constitutively active in the cells, keeps β -catenin phosphorylated on serine and threonine residues, and controls its proteosomal-mediated degradation. This raises the question whether inhibition of GSK3β activity, β -catenin stabilization, and therefore, pharmacological activation of endogenous neurogenesis would be a plausible therapeutic strategy for treating AD patients. In this chapter, we herein review the Wnt/β-catenin signaling and evaluate the strategy of inhibiting GSK3β in the disease.

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