TY - JOUR
T1 - Pharmacophore-based models for therapeutic drugs against phosphorylated tau in Alzheimer's disease
AU - Pradeepkiran, Jangampalli Adi
AU - Reddy, Arubala P.
AU - Reddy, P. Hemachandra
N1 - Funding Information:
This work was supported by NIH grantsAG042178, AG47812 and NS105473; the Garrison Family Foundation; the CH Foundation; and a Sex and Gender Alzheimer's Association (SAGA) grant (PHR). The present work is also supported by Alzheimer's Association New Investigator Research Grant2016-NIRG-39787 and Center of Excellence for Translational Neuroscience and Therapeutics grant number PN-CTNT20115-AR and Sex and Gender Alzheimer's Association (SAGA) grant (to A.P.R.).
Funding Information:
This work was supported by NIH grants AG042178 , AG47812 and NS105473 ; the Garrison Family Foundation ; the CH Foundation ; and a Sex and Gender Alzheimer’s Association (SAGA) grant (PHR). The present work is also supported by Alzheimer’s Association New Investigator Research Grant 2016-NIRG-39787 and Center of Excellence for Translational Neuroscience and Therapeutics grant number PN-CTNT20115-AR and Sex and Gender Alzheimer’s Association (SAGA) grant (to A.P.R.).
Publisher Copyright:
© 2018 Elsevier Ltd
PY - 2019/2
Y1 - 2019/2
N2 - Phosphorylated tau (P-tau) has received much attention in the field of Alzheimer's disease (AD), as a potential therapeutic target owing to its involvement with synaptic damage and neuronal dysfunction. The continuous failure of amyloid β (Aβ)-targeted therapeutics highlights the urgency to consider alternative therapeutic strategies for AD. The present review describes the latest developments in tau biology and function. It also explains abnormal interactions between P-tau with Aβ and the mitochondrial fission protein Drp1, leading to excessive mitochondrial fragmentation and synaptic damage in AD neurons. This article also addresses 3D pharmacophore-based drug models designed to treat patients with AD and other tauopathies.
AB - Phosphorylated tau (P-tau) has received much attention in the field of Alzheimer's disease (AD), as a potential therapeutic target owing to its involvement with synaptic damage and neuronal dysfunction. The continuous failure of amyloid β (Aβ)-targeted therapeutics highlights the urgency to consider alternative therapeutic strategies for AD. The present review describes the latest developments in tau biology and function. It also explains abnormal interactions between P-tau with Aβ and the mitochondrial fission protein Drp1, leading to excessive mitochondrial fragmentation and synaptic damage in AD neurons. This article also addresses 3D pharmacophore-based drug models designed to treat patients with AD and other tauopathies.
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U2 - 10.1016/j.drudis.2018.11.005
DO - 10.1016/j.drudis.2018.11.005
M3 - Review article
C2 - 30453058
AN - SCOPUS:85057058371
SN - 1359-6446
VL - 24
SP - 616
EP - 623
JO - Drug Discovery Today
JF - Drug Discovery Today
IS - 2
ER -