Pharmacophore-based models for therapeutic drugs against phosphorylated tau in Alzheimer's disease

Jangampalli Adi Pradeepkiran, Arubala Reddy, P (Hemachandra) Reddy

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
JournalDrug Discovery Today
DOIs
StateAccepted/In press - Jan 1 2018
Externally publishedYes

Fingerprint

Alzheimer Disease
Pharmaceutical Preparations
Tauopathies
Mitochondrial Dynamics
Mitochondrial Proteins
Therapeutics
Amyloid
Neurons

ASJC Scopus subject areas

  • Pharmacology
  • Drug Discovery

Cite this

Pharmacophore-based models for therapeutic drugs against phosphorylated tau in Alzheimer's disease. / Pradeepkiran, Jangampalli Adi; Reddy, Arubala; Reddy, P (Hemachandra).

In: Drug Discovery Today, 01.01.2018.

Research output: Contribution to journalArticle

Pradeepkiran, Jangampalli Adi ; Reddy, Arubala ; Reddy, P (Hemachandra). / Pharmacophore-based models for therapeutic drugs against phosphorylated tau in Alzheimer's disease. In: Drug Discovery Today. 2018.
@article{264b03b9e0ed478d9203e7af1888be0d,
title = "Pharmacophore-based models for therapeutic drugs against phosphorylated tau in Alzheimer's disease",
abstract = "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.",
author = "Pradeepkiran, {Jangampalli Adi} and Arubala Reddy and Reddy, {P (Hemachandra)}",
year = "2018",
month = "1",
day = "1",
doi = "10.1016/j.drudis.2018.11.005",
language = "English (US)",
journal = "Drug Discovery Today",
issn = "1359-6446",
publisher = "Elsevier Limited",

}

TY - JOUR

T1 - Pharmacophore-based models for therapeutic drugs against phosphorylated tau in Alzheimer's disease

AU - Pradeepkiran, Jangampalli Adi

AU - Reddy, Arubala

AU - Reddy, P (Hemachandra)

PY - 2018/1/1

Y1 - 2018/1/1

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.

UR - http://www.scopus.com/inward/record.url?scp=85057058371&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85057058371&partnerID=8YFLogxK

U2 - 10.1016/j.drudis.2018.11.005

DO - 10.1016/j.drudis.2018.11.005

M3 - Article

C2 - 30453058

AN - SCOPUS:85057058371

JO - Drug Discovery Today

JF - Drug Discovery Today

SN - 1359-6446

ER -