PMID- 19925479
OWN - NLM
STAT- MEDLINE
DCOM- 20111122
LR  - 20211020
IS  - 1755-5949 (Electronic)
IS  - 1755-5930 (Print)
IS  - 1755-5930 (Linking)
VI  - 17
IP  - 4
DP  - 2011 Aug
TI  - TGF-beta1 pathway as a new target for neuroprotection in Alzheimer's disease.
PG  - 237-49
LID - 10.1111/j.1755-5949.2009.00115.x [doi]
AB  - Alzheimer's disease (AD) is a neurodegenerative disorder that affects more than 
      37 million people worldwide. Current drugs for AD are only symptomatic, but do 
      not interfere with the underlying pathogenic mechanisms of the disease. AD is 
      characterized by the presence of ss-amyloid (Abeta) plaques, neurofibrillary tangles, 
      and neuronal loss. The identification of the molecular determinants underlying AD 
      pathogenesis is a fundamental step to design new disease-modifying drugs. 
      Recently, a specific impairment of transforming-growth-factor-beta1 (TGF-beta1) 
      signaling pathway has been demonstrated in AD brain. The deficiency of TGF-beta1 
      signaling has been shown to increase both Abeta accumulation and Abeta-induced 
      neurodegeneration in AD models. The loss of function of TGF-ss1 pathway seems also 
      to contribute to tau pathology and neurofibrillary tangle formation. Growing 
      evidence suggests a neuroprotective role for TGF-beta1 against Abeta toxicity both in 
      vitro and in vivo models of AD. Different drugs, such as lithium or group II mGlu 
      receptor agonists are able to increase TGF-beta1 levels in the central nervous 
      system (CNS), and might be considered as new neuroprotective tools against 
      Abeta-induced neurodegeneration. In the present review, we examine the evidence for 
      a neuroprotective role of TGF-beta1 in AD, and discuss the TGF-beta1 signaling pathway 
      as a new pharmacological target for the treatment of AD.
CI  - (c) 2009 Blackwell Publishing Ltd.
FAU - Caraci, Filippo
AU  - Caraci F
AD  - Department of Pharmaceutical Sciences, University of Catania, Italy. 
      carafil@hotmail.com
FAU - Battaglia, Giuseppe
AU  - Battaglia G
FAU - Bruno, Valeria
AU  - Bruno V
FAU - Bosco, Paolo
AU  - Bosco P
FAU - Carbonaro, Viviana
AU  - Carbonaro V
FAU - Giuffrida, Maria Laura
AU  - Giuffrida ML
FAU - Drago, Filippo
AU  - Drago F
FAU - Sortino, Maria Angela
AU  - Sortino MA
FAU - Nicoletti, Ferdinando
AU  - Nicoletti F
FAU - Copani, Agata
AU  - Copani A
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20091119
PL  - England
TA  - CNS Neurosci Ther
JT  - CNS neuroscience & therapeutics
JID - 101473265
RN  - 0 (Neuroprotective Agents)
RN  - 0 (Transforming Growth Factor beta1)
SB  - IM
MH  - Alzheimer Disease/*drug therapy/metabolism
MH  - Humans
MH  - Neuroprotective Agents/*therapeutic use
MH  - Signal Transduction/physiology
MH  - Transforming Growth Factor beta1/metabolism/*therapeutic use
PMC - PMC6493850
COIS- All authors declare that no potential conflict of interest exists, including all 
      relevant financial interests in any company or institution that might benefit 
      from the publication.
EDAT- 2009/11/21 06:00
MHDA- 2011/12/13 00:00
PMCR- 2009/11/19
CRDT- 2009/11/21 06:00
PHST- 2009/11/21 06:00 [entrez]
PHST- 2009/11/21 06:00 [pubmed]
PHST- 2011/12/13 00:00 [medline]
PHST- 2009/11/19 00:00 [pmc-release]
AID - CNS115 [pii]
AID - 10.1111/j.1755-5949.2009.00115.x [doi]
PST - ppublish
SO  - CNS Neurosci Ther. 2011 Aug;17(4):237-49. doi: 10.1111/j.1755-5949.2009.00115.x. 
      Epub 2009 Nov 19.