PMID- 26682679
OWN - NLM
STAT- MEDLINE
DCOM- 20161104
LR  - 20200708
IS  - 1875-8908 (Electronic)
IS  - 1387-2877 (Print)
IS  - 1387-2877 (Linking)
VI  - 50
IP  - 2
DP  - 2016
TI  - Molecular Signaling Mechanisms of Natural and Synthetic Retinoids for Inhibition 
      of Pathogenesis in Alzheimer's Disease.
PG  - 335-52
LID - 10.3233/JAD-150450 [doi]
AB  - Retinoids, which are vitamin A derivatives, interact through retinoic acid 
      receptors (RARs) and retinoid X receptors (RXRs) and have profound effects on 
      several physiological and pathological processes in the brain. The presence of 
      retinoic acid signaling is extensively detected in the adult central nervous 
      system, including the amygdala, cortex, hypothalamus, hippocampus, and other 
      brain areas. Retinoids are primarily involved in neural patterning, 
      differentiation, and axon outgrowth. Retinoids also play a key role in the 
      preservation of the differentiated state of adult neurons. Impairment in retinoic 
      acid signaling can result in neurodegeneration and progression of Alzheimer's 
      disease (AD). Recent studies demonstrated severe deficiencies in spatial learning 
      and memory in mice during retinoic acid (vitamin A) deprivation indicating its 
      significance in preserving memory function. Defective cholinergic 
      neurotransmission plays an important role in cognitive deficits in AD. All-trans 
      retinoic acid is known to enhance the expression and activity of choline 
      acetyltransferase in neuronal cell lines. Activation of RAR and RXR is also known 
      to impede the pathogenesis of AD in mice by inhibiting accumulation of amyloids. 
      In addition, retinoids have been shown to inhibit the expression of chemokines 
      and pro-inflammatory cytokines in microglia and astrocytes, which are activated 
      in AD. In this review article, we have described the chemistry and molecular 
      signaling mechanisms of natural and synthetic retinoids and current 
      understandings of their therapeutic potentials in prevention of AD pathology.
FAU - Chakrabarti, Mrinmay
AU  - Chakrabarti M
AD  - Department of Pathology, Microbiology, and Immunology, University of South 
      Carolina School of Medicine, Columbia, SC, USA.
FAU - McDonald, Alexander J
AU  - McDonald AJ
AD  - Department of Pharmacology, Physiology, and Neuroscience, University of South 
      Carolina School of Medicine, Columbia, SC, USA.
FAU - Will Reed, J
AU  - Will Reed J
AD  - Department of Chemical Engineering, University of South Carolina, Columbia, SC, 
      USA.
FAU - Moss, Melissa A
AU  - Moss MA
AD  - Department of Chemical Engineering, University of South Carolina, Columbia, SC, 
      USA.
FAU - Das, Bhaskar C
AU  - Das BC
AD  - Division of Hematology and Oncology, University of Kansas Medical Center, Kansas 
      City, KS, USA.
FAU - Ray, Swapan K
AU  - Ray SK
AD  - Department of Pathology, Microbiology, and Immunology, University of South 
      Carolina School of Medicine, Columbia, SC, USA.
LA  - eng
GR  - P20 GM103641/GM/NIGMS NIH HHS/United States
GR  - P30 AG035982/AG/NIA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - Netherlands
TA  - J Alzheimers Dis
JT  - Journal of Alzheimer's disease : JAD
JID - 9814863
RN  - 0 (Retinoid X Receptors)
RN  - 0 (Retinoids)
RN  - 5688UTC01R (Tretinoin)
SB  - IM
MH  - Alzheimer Disease/*metabolism
MH  - Animals
MH  - Brain/*metabolism
MH  - Humans
MH  - Mice
MH  - Neurons/metabolism
MH  - Retinoid X Receptors/*metabolism
MH  - Retinoids/*metabolism
MH  - Signal Transduction/*physiology
MH  - Tretinoin/*metabolism
PMC - PMC4823019
MID - NIHMS772870
OTO - NOTNLM
OT  - Alzheimer's disease
OT  - amyloid-beta
OT  - neuroprotection
OT  - regenerative medicine
OT  - retinoids
EDAT- 2015/12/20 06:00
MHDA- 2016/11/05 06:00
PMCR- 2016/04/06
CRDT- 2015/12/20 06:00
PHST- 2015/12/20 06:00 [entrez]
PHST- 2015/12/20 06:00 [pubmed]
PHST- 2016/11/05 06:00 [medline]
PHST- 2016/04/06 00:00 [pmc-release]
AID - JAD150450 [pii]
AID - 10.3233/JAD-150450 [doi]
PST - ppublish
SO  - J Alzheimers Dis. 2016;50(2):335-52. doi: 10.3233/JAD-150450.