PMID- 24082824
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20131001
LR  - 20211021
IS  - 1389-2029 (Print)
IS  - 1875-5488 (Electronic)
IS  - 1389-2029 (Linking)
VI  - 14
IP  - 2
DP  - 2013 Apr
TI  - Role of the Transforming-Growth-Factor-beta1 Gene in Late-Onset Alzheimer's Disease: 
      Implications for the Treatment.
PG  - 147-56
LID - 10.2174/1389202911314020007 [doi]
AB  - Late-onset Alzheimer's disease (LOAD) is the most common form of dementia in the 
      elderly. LOAD has a complex and largely unknown etiology with strong genetic 
      determinants. Genetics of LOAD is known to involve several genetic risk factors 
      among which the Apolipoprotein E (APOE) gene seems to be the major recognized 
      genetic determinant. Recent efforts have been made to identify other genetic 
      factors involved in the pathophysiology of LOAD such as genes associated with a 
      deficit of neurotrophic factors in the AD brain. Genetic variations of 
      neurotrophic factors, such as brain-derived neurotrophic factor (BDNF), and 
      transforming-growth-factor-beta1 (TGF-beta1) are known to increase the risk to develop 
      LOAD and have also been related to depression susceptibility in LOAD. 
      Transforming-Growth-Factor-beta1 (TGF-beta1) is a neurotrophic factor that exerts 
      neuroprotective effects against ss-amyloid-induced neurodegeneration. Recent 
      evidence suggests that a specific impairment in the signaling of TGF-beta is an 
      early event in the pathogenesis of AD. TGF-beta1 protein levels are predominantly 
      under genetic control, and the TGF-beta1 gene, located on chromosome 19q13.1-3, 
      con-tains several single nucleotide polymorphisms (SNPs) upstream and in the 
      transcript region, such as the SNP at codon +10 (T/C) and +25 (G/C), which is 
      known to influence the level of expression of TGF-beta1. In the present review, we 
      summarize the current literature on genetic risk factors for LOAD, focusing on 
      the role of the TGF-beta1 gene, finally discussing the possible implications of 
      these genetic studies for the selection of patients eligible for neuroprotective 
      strategies in AD.
FAU - Bosco, Paolo
AU  - Bosco P
AD  - IRCCS Associazione Oasi Maria S.S. - Institute for Research on Mental Retardation 
      and Brain Aging, 94018 Troina, Enna, Italy.
FAU - Ferri, Raffaele
AU  - Ferri R
FAU - Salluzzo, Maria Grazia
AU  - Salluzzo MG
FAU - Castellano, Sabrina
AU  - Castellano S
FAU - Signorelli, Maria
AU  - Signorelli M
FAU - Nicoletti, Ferdinando
AU  - Nicoletti F
FAU - Nuovo, Santo Di
AU  - Nuovo SD
FAU - Drago, Filippo
AU  - Drago F
FAU - Caraci, Filippo
AU  - Caraci F
LA  - eng
PT  - Journal Article
PL  - United Arab Emirates
TA  - Curr Genomics
JT  - Current genomics
JID - 100960527
PMC - PMC3637679
OTO - NOTNLM
OT  - Alzheimer's disease
OT  - Depression
OT  - Drugs
OT  - Genetic polymorphism
OT  - Risk factor
OT  - Transforming-growth-factor-beta1.
EDAT- 2013/10/02 06:00
MHDA- 2013/10/02 06:01
PMCR- 2013/10/01
CRDT- 2013/10/02 06:00
PHST- 2012/06/30 00:00 [received]
PHST- 2013/01/31 00:00 [revised]
PHST- 2013/02/01 00:00 [accepted]
PHST- 2013/10/02 06:00 [entrez]
PHST- 2013/10/02 06:00 [pubmed]
PHST- 2013/10/02 06:01 [medline]
PHST- 2013/10/01 00:00 [pmc-release]
AID - CG-14-147 [pii]
AID - 10.2174/1389202911314020007 [doi]
PST - ppublish
SO  - Curr Genomics. 2013 Apr;14(2):147-56. doi: 10.2174/1389202911314020007.