PMID- 29357021
OWN - NLM
STAT- MEDLINE
DCOM- 20180919
LR  - 20240313
IS  - 2509-2723 (Electronic)
IS  - 2509-2715 (Print)
IS  - 2509-2723 (Linking)
VI  - 40
IP  - 1
DP  - 2018 Feb
TI  - Candidate molecular pathways of white matter vulnerability in the brain of normal 
      aging rhesus monkeys.
PG  - 31-47
LID - 10.1007/s11357-018-0006-2 [doi]
AB  - Mammalian aging is associated with decline in cognitive functions. Studies 
      searching for a cause of cognitive aging initially focused on neuronal loss but 
      quantitative investigations of rat, monkey, and human brain using stereology 
      demonstrated that in normal aging, unlike in neurodegenerative disease, neurons 
      are not lost. Instead, electron microscopic and MRI studies in normal aging 
      monkeys revealed age-related damage to myelin sheaths, loss of axons, and 
      reduction in white matter volume which correlates with cognitive impairments. 
      However, little is known about the cause of myelin defects or associated axon 
      loss. The present study investigates the effect of age on signaling pathways 
      between oligodendroglia and neurons using a custom PCR array to assess the 
      expression of 87 genes of interest in cortical gray matter and white matter from 
      the inferior parietal lobe (IPL) of normal rhesus monkeys ranging in age from 4.2 
      to 30.4 years old. From this array data, five target genes of interest were 
      selected for further analysis to confirm gene expression and measure protein 
      expression. The most interesting target gene identified is brain-derived 
      neurotrophic factor (BDNF), which was the only gene that was altered at both mRNA 
      and protein levels. In gray matter, BDNF mRNA was decreased. While the level of 
      the mature form of the protein was unchanged, there was a specific decrease in 
      the precursor form of BDNF. These alterations in the BDNF in gray matter could 
      contribute to the vulnerability and loss of the axons with age.
FAU - Robinson, Amy A
AU  - Robinson AA
AUID- ORCID: 0000-0002-7029-4775
AD  - Department of Pharmacology and Experimental Therapeutics, Boston University 
      School of Medicine, Boston, MA, 02118, USA. amyarobinson@gmail.com.
FAU - Abraham, Carmela R
AU  - Abraham CR
AD  - Department of Pharmacology and Experimental Therapeutics, Boston University 
      School of Medicine, Boston, MA, 02118, USA.
AD  - Department of Biochemistry, Boston University School of Medicine, Boston, MA, 
      02118, USA.
FAU - Rosene, Douglas L
AU  - Rosene DL
AD  - Department of Anatomy and Neurobiology, Boston University School of Medicine, 
      Boston, MA, 02118, USA.
AD  - Yerkes National Primate Research Center, Emory University, Atlanta, GA, 30322, 
      USA.
LA  - eng
GR  - R01 AG043640/AG/NIA NIH HHS/United States
GR  - P51 OD011132/OD/NIH HHS/United States
GR  - P01 AG000001/AG/NIA NIH HHS/United States
GR  - RF1 AG043640/AG/NIA NIH HHS/United States
GR  - P51 RR000165/RR/NCRR NIH HHS/United States
GR  - P01-AG000001/AG/NIA NIH HHS/United States
GR  - T32-GM008541/GM/NIGMS NIH HHS/United States
GR  - T32 GM008541/GM/NIGMS NIH HHS/United States
GR  - P51-RR00165/NIH Office of the Director/International
GR  - R01 AG042512/AG/NIA NIH HHS/United States
GR  - R01-AG042512/AG/NIA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20180122
PL  - Switzerland
TA  - Geroscience
JT  - GeroScience
JID - 101686284
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (RNA, Messenger)
RN  - 7171WSG8A2 (BDNF protein, human)
SB  - IM
MH  - Aging/*physiology
MH  - Animals
MH  - Biopsy, Needle
MH  - Brain/metabolism/*pathology
MH  - Brain-Derived Neurotrophic Factor/*genetics
MH  - Cognition/physiology
MH  - Cognitive Dysfunction/genetics/*metabolism
MH  - Female
MH  - Genetic Association Studies/methods
MH  - Immunohistochemistry
MH  - Macaca mulatta
MH  - Male
MH  - RNA, Messenger/genetics
MH  - Real-Time Polymerase Chain Reaction/methods
MH  - Reference Values
MH  - White Matter/metabolism
PMC - PMC5832663
OTO - NOTNLM
OT  - Aging
OT  - BDNF
OT  - Gene expression
OT  - Parietal cortex
OT  - Protein expression
OT  - White matter
COIS- All procedures were in accord with NIH guidelines and approved by the 
      Institutional Animal Care and Use Committee of BUMC.
EDAT- 2018/01/23 06:00
MHDA- 2018/09/20 06:00
PMCR- 2018/01/22
CRDT- 2018/01/23 06:00
PHST- 2017/05/22 00:00 [received]
PHST- 2018/01/08 00:00 [accepted]
PHST- 2018/01/23 06:00 [pubmed]
PHST- 2018/09/20 06:00 [medline]
PHST- 2018/01/23 06:00 [entrez]
PHST- 2018/01/22 00:00 [pmc-release]
AID - 10.1007/s11357-018-0006-2 [pii]
AID - 6 [pii]
AID - 10.1007/s11357-018-0006-2 [doi]
PST - ppublish
SO  - Geroscience. 2018 Feb;40(1):31-47. doi: 10.1007/s11357-018-0006-2. Epub 2018 Jan 
      22.