PMID- 29438781
OWN - NLM
STAT- MEDLINE
DCOM- 20190118
LR  - 20190118
IS  - 1096-1186 (Electronic)
IS  - 1043-6618 (Linking)
VI  - 130
DP  - 2018 Apr
TI  - Neurobiological links between depression and AD: The role of TGF-beta1 signaling as 
      a new pharmacological target.
PG  - 374-384
LID - S1043-6618(17)31600-6 [pii]
LID - 10.1016/j.phrs.2018.02.007 [doi]
AB  - In the last several years a large number of studies have demonstrated the 
      neurobiological and clinical continuum between depression and Alzheimer's disease 
      (AD). Depression is a risk factor for the development of AD, and the presence of 
      depressive symptoms significantly increases the conversion of Mild Cognitive 
      Impairment (MCI) into AD. Common pathophysiological events have been identified 
      in depression and AD, including neuroinflammation with an aberrant Tumor Necrosis 
      Factor-alpha (TNF-alpha) signaling, and an impairment of Brain-Derived Neurotrophic 
      Factor (BDNF) and Transforming-Growth-Factor-beta1 (TGF-beta1) signaling. TGF-beta1 is an 
      anti-inflammatory cytokine that exerts neuroprotective effects against amyloid-beta 
      (Abeta)-induced neurodegeneration, and it has a key role in memory formation and 
      synaptic plasticity. TGF-beta1 plasma levels are reduced in major depressed patients 
      (MDD), correlate with depression severity, and significantly contribute to 
      treatment resistance in MDD. The deficit of Smad-dependent TGF-beta1 signaling is 
      also an early event in AD pathogenesis, which contributes to inflammaging and 
      cognitive decline in AD. A long-term treatment with antidepressants such as 
      selective-serotonin-reuptake inhibitors (SSRIs) is known to reduce the risk of AD 
      in patients with depression and, SSRIs, such as fluoxetine, increase the release 
      of TGF-beta1 from astrocytes and exert relevant neuroprotective effects in 
      experimental models of AD. We propose the TGF-beta1 signaling pathway as a common 
      pharmacological target in depression and AD, and discuss the potential rescue of 
      TGF-beta1 signaling by antidepressants as a way to prevent the transition from 
      depression to AD.
CI  - Copyright (c) 2018 Elsevier Ltd. All rights reserved.
FAU - Caraci, Filippo
AU  - Caraci F
AD  - Department of Drug Sciences, University of Catania, Catania, Italy; Oasi Research 
      Institute-IRCCS, Troina, Italy. Electronic address: fcaraci@unict.it.
FAU - Spampinato, Simona Federica
AU  - Spampinato SF
AD  - Department of Biomedical and Biotechnological Sciences, University of Catania, 
      Catania, Italy.
FAU - Morgese, Maria Grazia
AU  - Morgese MG
AD  - Department of Clinical and Experimental Medicine, University of Foggia, Foggia, 
      Italy.
FAU - Tascedda, Fabio
AU  - Tascedda F
AD  - Department of Life Sciences, University of Modena and Reggio Emilia, Modena, 
      Italy.
FAU - Salluzzo, Maria Grazia
AU  - Salluzzo MG
AD  - Oasi Research Institute-IRCCS, Troina, Italy.
FAU - Giambirtone, Maria Concetta
AU  - Giambirtone MC
AD  - Oasi Research Institute-IRCCS, Troina, Italy.
FAU - Caruso, Giuseppe
AU  - Caruso G
AD  - Oasi Research Institute-IRCCS, Troina, Italy.
FAU - Munafo, Antonio
AU  - Munafo A
AD  - Department of Drug Sciences, University of Catania, Catania, Italy.
FAU - Torrisi, Sebastiano Alfio
AU  - Torrisi SA
AD  - Department of Biomedical and Biotechnological Sciences, University of Catania, 
      Catania, Italy.
FAU - Leggio, Gian Marco
AU  - Leggio GM
AD  - Department of Biomedical and Biotechnological Sciences, University of Catania, 
      Catania, Italy.
FAU - Trabace, Luigia
AU  - Trabace L
AD  - Department of Clinical and Experimental Medicine, University of Foggia, Foggia, 
      Italy.
FAU - Nicoletti, Ferdinando
AU  - Nicoletti F
AD  - I.N.M. Neuromed, Localita Camerelle, Pozzilli, Italy; Department of Human 
      Physiology and Pharmacology, University of Rome Sapienza, Rome, Italy.
FAU - Drago, Filippo
AU  - Drago F
AD  - Department of Biomedical and Biotechnological Sciences, University of Catania, 
      Catania, Italy.
FAU - Sortino, Maria Angela
AU  - Sortino MA
AD  - Department of Biomedical and Biotechnological Sciences, University of Catania, 
      Catania, Italy.
FAU - Copani, Agata
AU  - Copani A
AD  - Department of Drug Sciences, University of Catania, Catania, Italy; I.B.B., 
      CNR-Catania, Catania, Italy.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20180210
PL  - Netherlands
TA  - Pharmacol Res
JT  - Pharmacological research
JID - 8907422
RN  - 0 (Transforming Growth Factor beta1)
SB  - IM
MH  - Alzheimer Disease/*drug therapy/epidemiology/metabolism
MH  - Animals
MH  - Cognitive Dysfunction/metabolism
MH  - Depression/*drug therapy/epidemiology/metabolism
MH  - Humans
MH  - Signal Transduction
MH  - Transforming Growth Factor beta1/*metabolism
OTO - NOTNLM
OT  - Alzheimer's disease
OT  - Amyloid-beta
OT  - Antidepressants
OT  - Depression
OT  - Transforming-Growth-Factor-beta1
EDAT- 2018/02/14 06:00
MHDA- 2019/01/19 06:00
CRDT- 2018/02/14 06:00
PHST- 2017/12/12 00:00 [received]
PHST- 2018/02/03 00:00 [revised]
PHST- 2018/02/07 00:00 [accepted]
PHST- 2018/02/14 06:00 [pubmed]
PHST- 2019/01/19 06:00 [medline]
PHST- 2018/02/14 06:00 [entrez]
AID - S1043-6618(17)31600-6 [pii]
AID - 10.1016/j.phrs.2018.02.007 [doi]
PST - ppublish
SO  - Pharmacol Res. 2018 Apr;130:374-384. doi: 10.1016/j.phrs.2018.02.007. Epub 2018 
      Feb 10.