PMID- 31244658
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20201001
IS  - 1663-9812 (Print)
IS  - 1663-9812 (Electronic)
IS  - 1663-9812 (Linking)
VI  - 10
DP  - 2019
TI  - Astrocyte Function Is Affected by Aging and Not Alzheimer's Disease: A 
      Preliminary Investigation in Hippocampi of 3xTg-AD Mice.
PG  - 644
LID - 10.3389/fphar.2019.00644 [doi]
LID - 644
AB  - Old age is a risk factor for Alzheimer's disease (AD), which is characterized by 
      hippocampal impairment together with substantial changes in glial cell functions. 
      Are these alterations due to the disease progression or are they a consequence of 
      aging? To start addressing this issue, we studied the expression of specific 
      astrocytic and microglial structural and functional proteins in a validated 
      transgenic model of AD (3xTg-AD). These mice develop both amyloid plaques and 
      neurofibrillary tangles, and initial signs of the AD-like pathology have been 
      documented as early as three months of age. We compared male 3xTg-AD mice at 6 
      and 12 months of age with their wild-type age-matched counterparts. We also 
      investigated neurons by examining the expression of both the 
      microtubule-associated protein 2 (MAP2), a neuronal structural protein, and the 
      brain-derived neurotrophic factor (BDNF). The latter is indeed a crucial 
      indicator for synaptic plasticity and neurogenesis/neurodegeneration. Our results 
      show that astrocytes are more susceptible to aging than microglia, regardless of 
      mouse genotype. Moreover, we discovered significant age-dependent alterations in 
      the expression of proteins responsible for astrocyte-astrocyte and 
      astrocyte-neuron communication, as well as a significant age-dependent decline in 
      BDNF expression. Our data promote further research on the unexplored role of 
      astroglia in both physiological and pathological aging.
FAU - Bronzuoli, Maria Rosanna
AU  - Bronzuoli MR
AD  - Department of Physiology and Pharmacology "V. Erspamer," Sapienza University of 
      Rome, Rome, Italy.
FAU - Facchinetti, Roberta
AU  - Facchinetti R
AD  - Department of Physiology and Pharmacology "V. Erspamer," Sapienza University of 
      Rome, Rome, Italy.
FAU - Valenza, Marta
AU  - Valenza M
AD  - Department of Physiology and Pharmacology "V. Erspamer," Sapienza University of 
      Rome, Rome, Italy.
AD  - Epitech Group SpA, Saccolongo, Italy.
FAU - Cassano, Tommaso
AU  - Cassano T
AD  - Department of Clinical and Experimental Medicine, University of Foggia, Foggia, 
      Italy.
FAU - Steardo, Luca
AU  - Steardo L
AD  - Department of Physiology and Pharmacology "V. Erspamer," Sapienza University of 
      Rome, Rome, Italy.
FAU - Scuderi, Caterina
AU  - Scuderi C
AD  - Department of Physiology and Pharmacology "V. Erspamer," Sapienza University of 
      Rome, Rome, Italy.
LA  - eng
PT  - Journal Article
DEP - 20190606
PL  - Switzerland
TA  - Front Pharmacol
JT  - Frontiers in pharmacology
JID - 101548923
PMC - PMC6562169
OTO - NOTNLM
OT  - 3xTg-AD mouse
OT  - AQP4
OT  - Alzheimer's disease
OT  - S100B
OT  - aging
OT  - astrocyte
OT  - brain-derived neurotrophic factor
OT  - connexin-43
EDAT- 2019/06/28 06:00
MHDA- 2019/06/28 06:01
PMCR- 2019/06/06
CRDT- 2019/06/28 06:00
PHST- 2019/02/12 00:00 [received]
PHST- 2019/05/17 00:00 [accepted]
PHST- 2019/06/28 06:00 [entrez]
PHST- 2019/06/28 06:00 [pubmed]
PHST- 2019/06/28 06:01 [medline]
PHST- 2019/06/06 00:00 [pmc-release]
AID - 10.3389/fphar.2019.00644 [doi]
PST - epublish
SO  - Front Pharmacol. 2019 Jun 6;10:644. doi: 10.3389/fphar.2019.00644. eCollection 
      2019.