PMID- 24582848
OWN - NLM
STAT- MEDLINE
DCOM- 20141209
LR  - 20140402
IS  - 1873-5177 (Electronic)
IS  - 0091-3057 (Linking)
VI  - 120
DP  - 2014 May
TI  - Retinoids as potential targets for Alzheimer's disease.
PG  - 117-23
LID - S0091-3057(14)00068-9 [pii]
LID - 10.1016/j.pbb.2014.02.016 [doi]
AB  - Vitamin A and its derivatives, the retinoids, modulate several physiological and 
      pathological processes through their interactions with nuclear retinoid receptor 
      proteins termed as retinoic acid receptors (RARs) and retinoid X receptors 
      (RXRs). An increasing body of evidence signifies the existence of retinoid 
      signaling in diverse brain areas including cortex, amygdala, hypothalamus, 
      hippocampus, and striatum suggesting its involvement in adult brain functions. 
      Defective retinoid signaling has been evidenced in the pathology of Alzheimer's 
      disease. Reports demonstrate that vitamin A deprived mice exhibit serious defects 
      in spatial learning and memory signifying its importance in the maintenance of 
      memory functions. Retinoid signaling impacts the development of AD pathology 
      through multiple pathways. Ligand activation of RAR and RXR in APP/PS1 transgenic 
      mice ameliorated the symptoms of AD and reduced amyloid accumulation and tau 
      hyperphosphorylation. Retinoids also reduce the production of pro-inflammatory 
      cytokines and chemokines by astrocytes and the microglia. Studies also suggest 
      that neuronal cell lines treated with retinoid agonists exhibit an up-regulation 
      in the expression and activity of choline acetyltransferase (ChAT). Reports 
      depict that retinoic acid isomers enhance, the expression of genes linked with 
      cholesterol efflux e.g. apoe, abca-1 and abcg-1 proteins in astrocytes. 
      Furthermore numerous studies also indicate antioxidant potential of retinoids. 
      Through this review we concisely summarize the biology of retinoids, emphasizing 
      on their probable neuroprotective mechanisms that will help to elucidate the 
      pivotal role of these receptors in AD pathology.
CI  - Copyright (c) 2014 Elsevier Inc. All rights reserved.
FAU - Sodhi, Rupinder K
AU  - Sodhi RK
AD  - Pharmacology Division, Department of Pharmaceutical Sciences and Drug Research, 
      Faculty of Medicine, Punjabi University, Patiala, 147002 Punjab, India.
FAU - Singh, Nirmal
AU  - Singh N
AD  - Pharmacology Division, Department of Pharmaceutical Sciences and Drug Research, 
      Faculty of Medicine, Punjabi University, Patiala, 147002 Punjab, India. 
      Electronic address: nirmal_puru@rediffmail.com.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20140226
PL  - United States
TA  - Pharmacol Biochem Behav
JT  - Pharmacology, biochemistry, and behavior
JID - 0367050
RN  - 0 (Neuroprotective Agents)
RN  - 0 (Retinoids)
SB  - IM
MH  - Alzheimer Disease/*drug therapy/physiopathology
MH  - Animals
MH  - Brain/drug effects/physiopathology
MH  - Humans
MH  - Neuroprotective Agents/pharmacology
MH  - Retinoids/pharmacology/*therapeutic use
MH  - Signal Transduction/drug effects
OTO - NOTNLM
OT  - Alzheimer's disease
OT  - Amyloid
OT  - ApoE
OT  - Oxidative stress
OT  - Retinoids
EDAT- 2014/03/04 06:00
MHDA- 2014/12/15 06:00
CRDT- 2014/03/04 06:00
PHST- 2013/05/17 00:00 [received]
PHST- 2014/02/17 00:00 [revised]
PHST- 2014/02/20 00:00 [accepted]
PHST- 2014/03/04 06:00 [entrez]
PHST- 2014/03/04 06:00 [pubmed]
PHST- 2014/12/15 06:00 [medline]
AID - S0091-3057(14)00068-9 [pii]
AID - 10.1016/j.pbb.2014.02.016 [doi]
PST - ppublish
SO  - Pharmacol Biochem Behav. 2014 May;120:117-23. doi: 10.1016/j.pbb.2014.02.016. 
      Epub 2014 Feb 26.