PMID- 24679124
OWN - NLM
STAT- MEDLINE
DCOM- 20141006
LR  - 20240321
IS  - 1478-811X (Electronic)
IS  - 1478-811X (Linking)
VI  - 12
DP  - 2014 Mar 28
TI  - Signaling pathway cross talk in Alzheimer's disease.
PG  - 23
LID - 10.1186/1478-811X-12-23 [doi]
AB  - Numerous studies suggest energy failure and accumulative intracellular waste play 
      a causal role in the pathogenesis of several neurodegenerative disorders and 
      Alzheimer's disease (AD) in particular. AD is characterized by extracellular 
      amyloid deposits, intracellular neurofibrillary tangles, cholinergic deficits, 
      synaptic loss, inflammation and extensive oxidative stress. These pathobiological 
      changes are accompanied by significant behavioral, motor, and cognitive 
      impairment leading to accelerated mortality. Currently, the potential role of 
      several metabolic pathways associated with AD, including Wnt signaling, 5' 
      adenosine monophosphate-activated protein kinase (AMPK), mammalian target of 
      rapamycin (mTOR), Sirtuin 1 (Sirt1, silent mating-type information regulator 2 
      homolog 1), and peroxisome proliferator-activated receptor gamma co-activator 1-alpha 
      (PGC-1alpha) have widened, with recent discoveries that they are able to modulate 
      several pathological events in AD. These include reduction of amyloid-beta 
      aggregation and inflammation, regulation of mitochondrial dynamics, and increased 
      availability of neuronal energy. This review aims to highlight the involvement of 
      these new set of signaling pathways, which we have collectively termed 
      "anti-ageing pathways", for their potentiality in multi-target therapies against 
      AD where cellular metabolic processes are severely impaired.
FAU - Godoy, Juan A
AU  - Godoy JA
FAU - Rios, Juvenal A
AU  - Rios JA
FAU - Zolezzi, Juan M
AU  - Zolezzi JM
FAU - Braidy, Nady
AU  - Braidy N
FAU - Inestrosa, Nibaldo C
AU  - Inestrosa NC
AD  - Centro de Envejecimiento y Regeneracion (CARE); Departamento de Biologia Celular 
      y Molecular; Facultad de Ciencias Biologicas, Pontificia Universidad Catolica de 
      Chile, Av, Alameda 340, Santiago, Chile. ninestrosa@bio.puc.cl.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20140328
PL  - England
TA  - Cell Commun Signal
JT  - Cell communication and signaling : CCS
JID - 101170464
RN  - 0 (Transcription Factors)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - EC 2.7.11.31 (AMP-Activated Protein Kinases)
RN  - EC 3.5.1.- (Sirtuin 1)
SB  - IM
MH  - AMP-Activated Protein Kinases/metabolism
MH  - Alzheimer Disease/*metabolism
MH  - Animals
MH  - Humans
MH  - Sirtuin 1/metabolism
MH  - TOR Serine-Threonine Kinases/metabolism
MH  - Transcription Factors/metabolism
MH  - *Wnt Signaling Pathway
PMC - PMC3977891
EDAT- 2014/04/01 06:00
MHDA- 2014/10/07 06:00
PMCR- 2014/03/28
CRDT- 2014/04/01 06:00
PHST- 2014/01/30 00:00 [received]
PHST- 2014/03/11 00:00 [accepted]
PHST- 2014/04/01 06:00 [entrez]
PHST- 2014/04/01 06:00 [pubmed]
PHST- 2014/10/07 06:00 [medline]
PHST- 2014/03/28 00:00 [pmc-release]
AID - 1478-811X-12-23 [pii]
AID - 10.1186/1478-811X-12-23 [doi]
PST - epublish
SO  - Cell Commun Signal. 2014 Mar 28;12:23. doi: 10.1186/1478-811X-12-23.