PMID- 23600400
OWN - NLM
STAT- MEDLINE
DCOM- 20130702
LR  - 20211021
IS  - 1365-2796 (Electronic)
IS  - 0954-6820 (Print)
IS  - 0954-6820 (Linking)
VI  - 273
IP  - 5
DP  - 2013 May
TI  - Synaptic dysfunction in human immunodeficiency virus type-1-positive subjects: 
      inflammation or impaired neuronal plasticity?
PG  - 454-65
LID - 10.1111/joim.12050 [doi]
AB  - Many people infected with the human immunodeficiency virus type-1 (HIV) exhibit 
      mild or severe neurological problems, termed HIV-associated neurocognitive 
      disorder (HAND), even when receiving antiretroviral therapy. Thus, novel 
      adjunctive therapies must be developed to overcome the neurotoxic effect of HIV. 
      New therapies require a better understanding of the molecular and cellular 
      mechanisms of HIV-induced neurotoxicity and the risk factors that, besides 
      inflammation and T-cell depletion and drugs of abuse, render the central nervous 
      system (CNS) a target of HIV-induced neurotoxicity. HIV appears to impair 
      neuronal plasticity, which refers to the innate ability of the CNS respond to 
      injury and promote recovery of function. The availability of brain-derived 
      neurotrophic factor (BDNF), a potent neurotrophic factor that is present in 
      abundance in the adult brain, is essential for neuronal plasticity. BDNF acts 
      through a receptor system composed of Trk and p75NTR. Here, we present 
      experimental evidence that some of the clinical features of HIV-mediated 
      neurological impairment could result from altered BDNF/TrkB/p75NTR regulation and 
      function.
CI  - (c) 2013 The Association for the Publication of the Journal of Internal Medicine.
FAU - Avdoshina, V
AU  - Avdoshina V
AD  - Laboratory of Preclinical Neurobiology, Department of Neuroscience, Georgetown 
      University Medical Center, Washington, DC, USA.
FAU - Bachis, A
AU  - Bachis A
FAU - Mocchetti, I
AU  - Mocchetti I
LA  - eng
GR  - R01 DA026174/DA/NIDA NIH HHS/United States
GR  - 1R21 NS074916/NS/NINDS NIH HHS/United States
GR  - 1R01 NS079172/NS/NINDS NIH HHS/United States
GR  - R01 NS079172/NS/NINDS NIH HHS/United States
GR  - 1R01 DA026174/DA/NIDA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Review
PL  - England
TA  - J Intern Med
JT  - Journal of internal medicine
JID - 8904841
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (NGFR protein, human)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (Receptors, Nerve Growth Factor)
RN  - EC 2.7.10.1 (Receptor, trkB)
SB  - IM
MH  - AIDS Dementia Complex/physiopathology
MH  - Axonal Transport
MH  - Brain-Derived Neurotrophic Factor/*metabolism
MH  - Evidence-Based Medicine
MH  - Gene Expression Regulation, Viral
MH  - HIV Seropositivity/complications/diagnosis/metabolism/*physiopathology
MH  - *HIV-1/isolation & purification
MH  - Humans
MH  - Inflammation/complications
MH  - Nerve Tissue Proteins/*metabolism
MH  - *Neuronal Plasticity
MH  - Receptor, trkB/*metabolism
MH  - Receptors, Nerve Growth Factor/*metabolism
MH  - Risk Factors
MH  - Severity of Illness Index
MH  - *Synapses
MH  - Synaptic Transmission
PMC - PMC3633109
MID - NIHMS447313
COIS- Conflict of interest statement None of the authors has any financial or other 
      conflicts of interest.
EDAT- 2013/04/23 06:00
MHDA- 2013/07/03 06:00
PMCR- 2014/05/01
CRDT- 2013/04/23 06:00
PHST- 2013/04/23 06:00 [entrez]
PHST- 2013/04/23 06:00 [pubmed]
PHST- 2013/07/03 06:00 [medline]
PHST- 2014/05/01 00:00 [pmc-release]
AID - 10.1111/joim.12050 [doi]
PST - ppublish
SO  - J Intern Med. 2013 May;273(5):454-65. doi: 10.1111/joim.12050.