PMID- 26511378
OWN - NLM
STAT- MEDLINE
DCOM- 20160926
LR  - 20151215
IS  - 1879-0712 (Electronic)
IS  - 0014-2999 (Linking)
VI  - 769
DP  - 2015 Dec 15
TI  - Antidepressants for neuroprotection in Huntington's disease: A review.
PG  - 33-42
LID - S0014-2999(15)30314-9 [pii]
LID - 10.1016/j.ejphar.2015.10.033 [doi]
AB  - Huntington Disease (HD), which is characterized by abnormal dance-like movements, 
      is a neurodegenerative disorder caused by a genetic mutation that results in an 
      expanded polyglutamine stretch in the NH2 terminus of huntingtin protein (HTT). 
      The principal neuropathological hallmarks of disease include loss of striatal and 
      cortical projection neurons. HTT is ubiquitously expressed and is implicated in 
      several cellular functions including neurogenesis, cell trafficking and 
      brain-derived neurotrophic factor (BDNF) production. Major depression is the most 
      common symptom among pre-symptomatic HD carriers and numerous pieces of 
      preclinical evidence have suggested the use of antidepressants in HD not only 
      elevates mood but also slows down the disease progression by activating different 
      neuroprotective mechanism like BDNF/TrkB pathway, MAPK/ERK signalling, 
      neurogenesis and Wnt signalling. HTT plays major role in neurogenesis, a 
      physiological phenomenon that is implicated in some of the behavioral effects of 
      antidepressants. Currently, there is no clinically available treatment that can 
      halt or slow down the progression of HD except tetrabenazine (the only FDA 
      approved drug); however, this drug also induces depression and sedation in 
      patients. In this review, a brief discussion has been made about the mutant HTT 
      that induced various cellular and molecular mechanisms underlying behavioral 
      disorders in HD. Further, an attempt has been made to understand the various 
      cellular mechanisms involved in mediating the neuroprotective effects of 
      antidepressants in HD.
CI  - Copyright (c) 2015 Elsevier B.V. All rights reserved.
FAU - Jamwal, Sumit
AU  - Jamwal S
AD  - Neuropharmacology Division, I. S. F. College of Pharmacy, Moga 142001, Punjab, 
      India; Research Scholar, I. K. Gujral Punjab Technical University, Jalandhar, 
      Punjab, India.
FAU - Kumar, Puneet
AU  - Kumar P
AD  - Neuropharmacology Division, I. S. F. College of Pharmacy, Moga 142001, Punjab, 
      India. Electronic address: punnubansal79@gmail.com.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20151025
PL  - Netherlands
TA  - Eur J Pharmacol
JT  - European journal of pharmacology
JID - 1254354
RN  - 0 (Antidepressive Agents)
RN  - 0 (Neuroprotective Agents)
SB  - IM
MH  - Animals
MH  - Antidepressive Agents/*pharmacology/therapeutic use
MH  - Humans
MH  - Huntington Disease/*drug therapy/etiology/metabolism/pathology
MH  - Neuroprotective Agents/*pharmacology/therapeutic use
OTO - NOTNLM
OT  - Antidepressants
OT  - Brain derived neurotrophic factor
OT  - Huntingtin protein
OT  - Huntington's disease
OT  - MAPK-ERK signalling
OT  - Wnt-GSK-3beta Signalling
EDAT- 2015/10/30 06:00
MHDA- 2016/09/27 06:00
CRDT- 2015/10/30 06:00
PHST- 2015/06/24 00:00 [received]
PHST- 2015/10/07 00:00 [revised]
PHST- 2015/10/19 00:00 [accepted]
PHST- 2015/10/30 06:00 [entrez]
PHST- 2015/10/30 06:00 [pubmed]
PHST- 2016/09/27 06:00 [medline]
AID - S0014-2999(15)30314-9 [pii]
AID - 10.1016/j.ejphar.2015.10.033 [doi]
PST - ppublish
SO  - Eur J Pharmacol. 2015 Dec 15;769:33-42. doi: 10.1016/j.ejphar.2015.10.033. Epub 
      2015 Oct 25.