Neural Regeneration Research ›› 2020, Vol. 15 ›› Issue (12): 2245-2246.doi: 10.4103/1673-5374.284986

Previous Articles     Next Articles

Activation of tyrosine phosphatases in the progression of Alzheimer’s disease

Alexandre F. R. Stewart1, Hsiao-Huei Chen2   

  1. 1 University of Ottawa Heart Institute, Ottawa, Canada
    2 Ottawa Hospital Research Institute, Ottawa, Canada 
  • Online:2020-12-15 Published:2020-08-04
  • Contact: Alexandre F. R. Stewart, PhD,astewart@ottawaheart.ca; Hsiao-Huei Chen, PhD, hchen@uottawa.ca.
  • Supported by:
    This work was supported by grants from the Heart and Stroke Foundation of Canada (to HHC, G-13-0002596 & G-18-0022157; to AFRS, G-16-00014085), the Natural Science and Engineering Research Council of Canada (to HHC, RGPIN/06212-2014; to AFRS, RGPIN/2016-04985) and the Canadian Institutes of Health Research (HHC, 201610PJT). HHC was also supported by a Mid-Career Investigator Award (grant No. 7506) from the Heart and Stroke Foundation of Ontario.

PDF

160

Abstract: Patients with Alzheimer’s disease (AD) have progressive memory loss, inability to reason, and display anxiety that accelerates disease progression. Evidence points to two deficits: 1) the brain fails to respond to insulin that regulates the formation of neuron connections required to store memories, and 2) deficits arise in the brain’s endogenous cannabinoid signaling that regulates mood and prevents anxiety (Aso and Ferrer, 2014). In addition, leptin signaling, important in regulating hypothalamic synaptic plasticity and cognitive function is also affected in AD (McGregor and Harvey, 2018). Until now, no single treatment targeting these three signaling deficits has been proposed. The tyrosine phosphatase PTP1B (Ptpn1) blocks brain insulin and leptin signaling (Pandey et al., 2013) and prevents endogenous cannabinoid production (Qin et al., 2015b) and is elevated in the brain of AD mice (Ricke et al., 2020). Thus, PTP1B is a plausible target for AD.