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Subject Item: _:vb46893550
rdf:type: n4:Section
dc:title: introduction
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Subject Item: _:vb46893551
rdf:type: n3:Context
rdf:value: Thus, some theories have been proposed to explain the aging process, as the theory of random accumulation of molecular damage in which cancer and aging should have similar origins although they seem opposite processes [>>2<<] and the hyperfunction theory that was first characterized by cellular hypertrophy followed by atrophy that try to explain the outgrowth of diabetes, cardiovascular disorders and chronic inflammation along the process [3, 4].
n3:mentions: n2:23746838

Subject Item: _:vb46893552
rdf:type: n3:Context
rdf:value: processes [2] and the hyperfunction theory that was first characterized by cellular hypertrophy followed by atrophy that try to explain the outgrowth of diabetes, cardiovascular disorders and chronic inflammation along the process [>>3<<, 4].
n3:mentions: n2:20157523

Subject Item: _:vb46893553
rdf:type: n3:Context
rdf:value: processes [2] and the hyperfunction theory that was first characterized by cellular hypertrophy followed by atrophy that try to explain the outgrowth of diabetes, cardiovascular disorders and chronic inflammation along the process [3, >>4<<].
n3:mentions: n2:23425777

Subject Item: _:vb46893554
rdf:type: n3:Context
rdf:value: stress and inflammation, leading to an increased susceptibility of neurons to death, coupled with a progressive decline in signaling molecules which can result in a decrease in motor and cognitive performances, especially memory [>>5<<]. Changes in learning and memory process reflect compromised hippocampal function and can really affect a personal quality of life and the ability to maintain an independent lifestyle [6, 7].
n3:mentions: n2:16006669

Subject Item: _:vb46893555
rdf:type: n3:Context
rdf:value: Changes in learning and memory process reflect compromised hippocampal function and can really affect a personal quality of life and the ability to maintain an independent lifestyle [>>6<<, 7].
n3:mentions: n2:23936746

Subject Item: _:vb46893556
rdf:type: n3:Context
rdf:value: Changes in learning and memory process reflect compromised hippocampal function and can really affect a personal quality of life and the ability to maintain an independent lifestyle [6, >>7<<].
n3:mentions: n2:14615299

Subject Item: _:vb46893557
rdf:type: n3:Context
rdf:value: However, brain aging has been considered a multifactorial process where a significant neuronal loss does not contribute by itself to an age-related cognitive decline [>>8<<, 9]. Nearly 40 years ago, neuroscientists began to correlate metabolic deregulation with the pathophysiology of neurological and psychiatric disorders due to Professor John P.
n3:mentions: n2:8790433

Subject Item: _:vb46893558
rdf:type: n3:Context
rdf:value: However, brain aging has been considered a multifactorial process where a significant neuronal loss does not contribute by itself to an age-related cognitive decline [8, >>9<<]. Nearly 40 years ago, neuroscientists began to correlate metabolic deregulation with the pathophysiology of neurological and psychiatric disorders due to Professor John P.
n3:mentions: n2:12379605

Subject Item: _:vb46893559
rdf:type: n3:Context
rdf:value: Nearly 40 years ago, neuroscientists began to correlate metabolic deregulation with the pathophysiology of neurological and psychiatric disorders due to Professor John P. Blass studies [>>10<<]. Since then, many proteins have been identified as crucial to intermediate the crosstalk between different signaling pathways involved either in metabolism and neuro-degenerative process, such as GSK-3β, which has been considered a
n3:mentions: n2:16944320

Subject Item: _:vb46893560
rdf:type: n3:Context
rdf:value: between different signaling pathways involved either in metabolism and neuro-degenerative process, such as GSK-3β, which has been considered a pro-inflammatory protein in addition to its fundamental role in insulin signaling pathway [>>10<<, 11].
n3:mentions: n2:16944320

Subject Item: _:vb46893561
rdf:type: n3:Context
rdf:value: different signaling pathways involved either in metabolism and neuro-degenerative process, such as GSK-3β, which has been considered a pro-inflammatory protein in addition to its fundamental role in insulin signaling pathway [10, >>11<<].
n3:mentions: n2:16007092

Subject Item: _:vb46893562
rdf:type: n3:Context
rdf:value: It is well known that human aging is accompanied by increased serum levels of pro-inflammatory cytokines, such as IL-1, IL-6 and TNF-α, what seems to be related to the immuno-senescence process [>>4<<–7, 12], as well as NF-кB signaling pathway [12–14], that can be considered as a key molecular system for brain inflammation leading to metabolic syndrome [15].
n3:mentions: n2:16006669 n2:23425777 n2:23936746 n2:14615299

Subject Item: _:vb46893563
rdf:type: n3:Context
rdf:value: It is well known that human aging is accompanied by increased serum levels of pro-inflammatory cytokines, such as IL-1, IL-6 and TNF-α, what seems to be related to the immuno-senescence process [4–7, >>12<<], as well as NF-кB signaling pathway [12–14], that can be considered as a key molecular system for brain inflammation leading to metabolic syndrome [15].
n3:mentions: n2:25553802

Subject Item: _:vb46893564
rdf:type: n3:Context
rdf:value: well known that human aging is accompanied by increased serum levels of pro-inflammatory cytokines, such as IL-1, IL-6 and TNF-α, what seems to be related to the immuno-senescence process [4–7, 12], as well as NF-кB signaling pathway [>>12<<–14], that can be considered as a key molecular system for brain inflammation leading to metabolic syndrome [15].
n3:mentions: n2:21483034 n2:25553802 n2:25553648

Subject Item: _:vb46893565
rdf:type: n3:Context
rdf:value: IL-6 and TNF-α, what seems to be related to the immuno-senescence process [4–7, 12], as well as NF-кB signaling pathway [12–14], that can be considered as a key molecular system for brain inflammation leading to metabolic syndrome [>>15<<].
n3:mentions: n2:23265946

Subject Item: _:vb46893566
rdf:type: n3:Context
rdf:value: NF-кB is constitutively expressed in the cytoplasm where it is retained by a family of inhibitory molecules termed inhibitor κB (IκB) [>>16<<]. NF-κB activity is attributed to the Rel/NF-κB protein family forming homo- and heterodimers through the combination of the subunits p65 (or RelA), p50, p52, c-Rel and RelB.
n3:mentions: n2:9597130

Subject Item: _:vb46893567
rdf:type: n3:Context
rdf:value: This transcription factor can be activated by lipopolysaccharide (LPS), cytokines such as tumor necrosis factor (TNF-α) and interleukin 1β (IL-1β), and reactive oxygen species [>>17<<, 18]. LPS, IL-1β, TNF-α, and reactive oxygen species all induce NF-κB by activating IκB kinases which phosphorylate IκBα, leading to its polyubiquitination and degradation at the proteasome 26S [19], allowing NF-κB to migrate to the
n3:mentions: n2:16623771

Subject Item: _:vb46893568
rdf:type: n3:Context
rdf:value: This transcription factor can be activated by lipopolysaccharide (LPS), cytokines such as tumor necrosis factor (TNF-α) and interleukin 1β (IL-1β), and reactive oxygen species [17, >>18<<]. LPS, IL-1β, TNF-α, and reactive oxygen species all induce NF-κB by activating IκB kinases which phosphorylate IκBα, leading to its polyubiquitination and degradation at the proteasome 26S [19], allowing NF-κB to migrate to the nucleus
n3:mentions: n2:16397579

Subject Item: _:vb46893569
rdf:type: n3:Context
rdf:value: LPS, IL-1β, TNF-α, and reactive oxygen species all induce NF-κB by activating IκB kinases which phosphorylate IκBα, leading to its polyubiquitination and degradation at the proteasome 26S [>>19<<], allowing NF-κB to migrate to the nucleus and to modulate the transcription of its target genes.
n3:mentions: n2:11983155

Subject Item: _:vb46893570
rdf:type: n3:Context
rdf:value: However, in the presence of glucocorticoids (GCs), the nuclear translocation of NF-κB can be prevented because GCs induce IκBα expression [>>20<<, 21], and can direct interact with the NF-κB p65 subunit, thereby blocking NF-κB-DNA-binding activity [22–24].
n3:mentions: n2:10964953

Subject Item: _:vb46893571
rdf:type: n3:Context
rdf:value: However, in the presence of glucocorticoids (GCs), the nuclear translocation of NF-κB can be prevented because GCs induce IκBα expression [20, >>21<<], and can direct interact with the NF-κB p65 subunit, thereby blocking NF-κB-DNA-binding activity [22–24].
n3:mentions: n2:10487715

Subject Item: _:vb46893572
rdf:type: n3:Context
rdf:value: in the presence of glucocorticoids (GCs), the nuclear translocation of NF-κB can be prevented because GCs induce IκBα expression [20, 21], and can direct interact with the NF-κB p65 subunit, thereby blocking NF-κB-DNA-binding activity [>>22<<–24]. In the presence of a chronic inflammatory process, glucocorticoids (GCs), that are well-known to be anti-inflammatory and immunosuppressive, can have pro-inflammatory effects in the brain [25, 26].
n3:mentions: n2:10969176 n2:9105673 n2:10935546

Subject Item: _:vb46893573
rdf:type: n3:Context
rdf:value: In the presence of a chronic inflammatory process, glucocorticoids (GCs), that are well-known to be anti-inflammatory and immunosuppressive, can have pro-inflammatory effects in the brain [>>25<<, 26].
n3:mentions: n2:16597735

Subject Item: _:vb46893574
rdf:type: n3:Context
rdf:value: In the presence of a chronic inflammatory process, glucocorticoids (GCs), that are well-known to be anti-inflammatory and immunosuppressive, can have pro-inflammatory effects in the brain [25, >>26<<].
n3:mentions: n2:20943909

Subject Item: _:vb46893575
rdf:type: n3:Context
rdf:value: Another very important hallmark of aging is the mTOR signaling pathway that has PI3K/AKT upstream [>>2<<, 12]. AKT (also known as protein kinase B) is a serine/threonine kinase that is believed to promote cell viability in many different cell types [27, 28], including neurons, by phosphorylating and thus inactivating downstream targets such
n3:mentions: n2:23746838

Subject Item: _:vb46893576
rdf:type: n3:Context
rdf:value: Another very important hallmark of aging is the mTOR signaling pathway that has PI3K/AKT upstream [2, >>12<<]. AKT (also known as protein kinase B) is a serine/threonine kinase that is believed to promote cell viability in many different cell types [27, 28], including neurons, by phosphorylating and thus inactivating downstream targets such as
n3:mentions: n2:25553802

Subject Item: _:vb46893577
rdf:type: n3:Context
rdf:value: AKT (also known as protein kinase B) is a serine/threonine kinase that is believed to promote cell viability in many different cell types [>>27<<, 28], including neurons, by phosphorylating and thus inactivating downstream targets such as the Ser/Thr kinase GSK-3β, forkhead transcription factor, pro-apoptotic Bcl-2 family members, and caspase-9 [29, 30].
n3:mentions: n2:11048732

Subject Item: _:vb46893578
rdf:type: n3:Context
rdf:value: AKT (also known as protein kinase B) is a serine/threonine kinase that is believed to promote cell viability in many different cell types [27, >>28<<], including neurons, by phosphorylating and thus inactivating downstream targets such as the Ser/Thr kinase GSK-3β, forkhead transcription factor, pro-apoptotic Bcl-2 family members, and caspase-9 [29, 30].
n3:mentions: n2:9005851

Subject Item: _:vb46893579
rdf:type: n3:Context
rdf:value: in many different cell types [27, 28], including neurons, by phosphorylating and thus inactivating downstream targets such as the Ser/Thr kinase GSK-3β, forkhead transcription factor, pro-apoptotic Bcl-2 family members, and caspase-9 [>>29<<, 30]. AKT is also known to regulate non-canonical NF-кB p52 processing by increasing the activity of IKKα [31].
n3:mentions: n2:11399427

Subject Item: _:vb46893580
rdf:type: n3:Context
rdf:value: many different cell types [27, 28], including neurons, by phosphorylating and thus inactivating downstream targets such as the Ser/Thr kinase GSK-3β, forkhead transcription factor, pro-apoptotic Bcl-2 family members, and caspase-9 [29, >>30<<]. AKT is also known to regulate non-canonical NF-кB p52 processing by increasing the activity of IKKα [31].
n3:mentions: n2:9812896

Subject Item: _:vb46893581
rdf:type: n3:Context
rdf:value: AKT is also known to regulate non-canonical NF-кB p52 processing by increasing the activity of IKKα [>>31<<].
n3:mentions: n2:23316192

Subject Item: _:vb46893582
rdf:type: n3:Context
rdf:value: Glycogen synthase kinase-3 (GSK-3) was first identified by its glycogen synthase phosphorylating activity [>>32<<] and some years later was described in the Central Nervous System (CNS) as a kinase of Tau protein [33, 34].
n3:mentions: n2:6249596

Subject Item: _:vb46893583
rdf:type: n3:Context
rdf:value: Glycogen synthase kinase-3 (GSK-3) was first identified by its glycogen synthase phosphorylating activity [32] and some years later was described in the Central Nervous System (CNS) as a kinase of Tau protein [>>33<<, 34]. The regulation of GSK-3 activity can be summarized in four key mechanisms which consist in the regulation of its phosphorylation state, its subcellular localization, the formation of protein complexes containing GSK-3, and the
n3:mentions: n2:7686508

Subject Item: _:vb46893584
rdf:type: n3:Context
rdf:value: Glycogen synthase kinase-3 (GSK-3) was first identified by its glycogen synthase phosphorylating activity [32] and some years later was described in the Central Nervous System (CNS) as a kinase of Tau protein [33, >>34<<]. The regulation of GSK-3 activity can be summarized in four key mechanisms which consist in the regulation of its phosphorylation state, its subcellular localization, the formation of protein complexes containing GSK-3, and the
n3:mentions: n2:15189333

Subject Item: _:vb46893585
rdf:type: n3:Context
rdf:value: can be summarized in four key mechanisms which consist in the regulation of its phosphorylation state, its subcellular localization, the formation of protein complexes containing GSK-3, and the phosphorylation state of its substrates [>>10<<]. Regarding phosphorylation, GSK-3 activity is inhibited through phosphorylation of serine 21 in α isoform and of serine 9 in β-isoform [35].
n3:mentions: n2:16944320

Subject Item: _:vb46893586
rdf:type: n3:Context
rdf:value: Regarding phosphorylation, GSK-3 activity is inhibited through phosphorylation of serine 21 in α isoform and of serine 9 in β-isoform [>>35<<]. When phosphorylated in the Ser9 residue, GSK-3β is inactivated, increasing the stabilized unphosphorylated state of β-CATENIN [36]. Thus, AKT/GSK-3β/β-CATENIN signaling plays a critical role in neuroinflammation and apoptosis of neurons
n3:mentions: n2:11035810

Subject Item: _:vb46893587
rdf:type: n3:Context
rdf:value: When phosphorylated in the Ser9 residue, GSK-3β is inactivated, increasing the stabilized unphosphorylated state of β-CATENIN [>>36<<]. Thus, AKT/GSK-3β/β-CATENIN signaling plays a critical role in neuroinflammation and apoptosis of neurons in several models of neurodegeneration [37, 38].
n3:mentions: n2:19298762

Subject Item: _:vb46893588
rdf:type: n3:Context
rdf:value: Thus, AKT/GSK-3β/β-CATENIN signaling plays a critical role in neuroinflammation and apoptosis of neurons in several models of neurodegeneration [>>37<<, 38].
n3:mentions: n2:22643085

Subject Item: _:vb46893589
rdf:type: n3:Context
rdf:value: Furthermore, β-CATENIN is a key component of the canonical WNT signaling pathway, acting as a transcriptional coactivator [>>37<<]. WNT proteins are secreted glycoproteins that bind to the cell surface Frizzled (Fz) receptor family and play an important role during development and in adult tissue homeostasis, but little is known about changes in β-CATENIN in
n3:mentions: n2:22643085

Subject Item: _:vb46893590
rdf:type: n3:Context
rdf:value: proteins are secreted glycoproteins that bind to the cell surface Frizzled (Fz) receptor family and play an important role during development and in adult tissue homeostasis, but little is known about changes in β-CATENIN in senescence [>>39<<]. WNT signaling pathway can be classified as canonical, when β-CATENIN is an important effector of the pathway, and non-canonical, when signaling happens independent of β-CATENIN activation [40].
n3:mentions: n2:23879250

Subject Item: _:vb46893591
rdf:type: n3:Context
rdf:value: WNT signaling pathway can be classified as canonical, when β-CATENIN is an important effector of the pathway, and non-canonical, when signaling happens independent of β-CATENIN activation [>>40<<].
n3:mentions: n2:17081971

Subject Item: _:vb46893592
rdf:type: n3:Context
rdf:value: In the absence of a WNT stimulus, cytoplasmic β-CATENIN is phosphorylated and degraded by proteasome [>>41<<, 42], due to the action of two kinases, GSK-3 and Casein kinase 1 alpha (CK1α), localized in two multidomain scaffolding proteins called AXIN and Adenomatous polyposis coli (APC), also known as destruction complex [42].
n3:mentions: n2:15473860

Subject Item: _:vb46893593
rdf:type: n3:Context
rdf:value: In the absence of a WNT stimulus, cytoplasmic β-CATENIN is phosphorylated and degraded by proteasome [41, >>42<<], due to the action of two kinases, GSK-3 and Casein kinase 1 alpha (CK1α), localized in two multidomain scaffolding proteins called AXIN and Adenomatous polyposis coli (APC), also known as destruction complex [42].
n3:mentions: n2:22952392

Subject Item: _:vb46893594
rdf:type: n3:Context
rdf:value: by proteasome [41, 42], due to the action of two kinases, GSK-3 and Casein kinase 1 alpha (CK1α), localized in two multidomain scaffolding proteins called AXIN and Adenomatous polyposis coli (APC), also known as destruction complex [>>42<<]. When WNT protein binds to the Fz receptor, it recruits the co-receptor LRP5/6 [43], and both Dishevelled (DVL) and AXIN proteins, which results in inhibition of β-CATENIN phosphorylation and thus ensuing its stabilization [42].
n3:mentions: n2:22952392

Subject Item: _:vb46893595
rdf:type: n3:Context
rdf:value: When WNT protein binds to the Fz receptor, it recruits the co-receptor LRP5/6 [>>43<<], and both Dishevelled (DVL) and AXIN proteins, which results in inhibition of β-CATENIN phosphorylation and thus ensuing its stabilization [42].
n3:mentions: n2:15084453

Subject Item: _:vb46893596
rdf:type: n3:Context
rdf:value: When WNT protein binds to the Fz receptor, it recruits the co-receptor LRP5/6 [43], and both Dishevelled (DVL) and AXIN proteins, which results in inhibition of β-CATENIN phosphorylation and thus ensuing its stabilization [>>42<<]. The stabilized β-CATENIN can also translocate to the nucleus where, together with Tcf/Lef proteins, it can control the transcription of specific genes like Axin 2, which acts as a negative-feedback regulator of WNT signaling [44].
n3:mentions: n2:22952392

Subject Item: _:vb46893597
rdf:type: n3:Context
rdf:value: The stabilized β-CATENIN can also translocate to the nucleus where, together with Tcf/Lef proteins, it can control the transcription of specific genes like Axin 2, which acts as a negative-feedback regulator of WNT signaling [>>44<<].
n3:mentions: n2:11940574

Subject Item: _:vb46893598
rdf:type: n3:Context
rdf:value: Recent studies also suggest an important role for DVL shaping neuronal projections [>>45<<] and in neural connectivity establishment [46], in a model of embryonic development of Caenorhabditis elegans and in Schmidtea mediterranea, respectively [47, 48].
n3:mentions: n2:25789082

Subject Item: _:vb46893599
rdf:type: n3:Context
rdf:value: Recent studies also suggest an important role for DVL shaping neuronal projections [45] and in neural connectivity establishment [>>46<<], in a model of embryonic development of Caenorhabditis elegans and in Schmidtea mediterranea, respectively [47, 48].
n3:mentions: n2:21282632

Subject Item: _:vb46893600
rdf:type: n3:Context
rdf:value: studies also suggest an important role for DVL shaping neuronal projections [45] and in neural connectivity establishment [46], in a model of embryonic development of Caenorhabditis elegans and in Schmidtea mediterranea, respectively [>>47<<, 48]. These actions of DVL can only be possible because DVL is a common intracellular mediator of canonical and non-canonical WNT signaling pathway, interacting with different proteins due to three conserved regions that are known as the
n3:mentions: n2:26460008

Subject Item: _:vb46893601
rdf:type: n3:Context
rdf:value: also suggest an important role for DVL shaping neuronal projections [45] and in neural connectivity establishment [46], in a model of embryonic development of Caenorhabditis elegans and in Schmidtea mediterranea, respectively [47, >>48<<]. These actions of DVL can only be possible because DVL is a common intracellular mediator of canonical and non-canonical WNT signaling pathway, interacting with different proteins due to three conserved regions that are known as the DIX,
n3:mentions: n2:7720076

Subject Item: _:vb46893602
rdf:type: n3:Context
rdf:value: can only be possible because DVL is a common intracellular mediator of canonical and non-canonical WNT signaling pathway, interacting with different proteins due to three conserved regions that are known as the DIX, PDZ and DEP domains [>>49<<]. Through these interactions, DVL can be found in various cellular compartments, as in complex with microtubules and actin cytoskeleton [50, 51] and in the nucleus, where interaction with c-Jun and β-CATENIN followed by formation of the
n3:mentions: n2:10507837

Subject Item: _:vb46893603
rdf:type: n3:Context
rdf:value: Through these interactions, DVL can be found in various cellular compartments, as in complex with microtubules and actin cytoskeleton [>>50<<, 51] and in the nucleus, where interaction with c-Jun and β-CATENIN followed by formation of the stable β-CATENIN/TCF complex was also demonstrated [52–54].
n3:mentions: n2:12384700

Subject Item: _:vb46893604
rdf:type: n3:Context
rdf:value: Through these interactions, DVL can be found in various cellular compartments, as in complex with microtubules and actin cytoskeleton [50, >>51<<] and in the nucleus, where interaction with c-Jun and β-CATENIN followed by formation of the stable β-CATENIN/TCF complex was also demonstrated [52–54].
n3:mentions: n2:14734535

Subject Item: _:vb46893605
rdf:type: n3:Context
rdf:value: cellular compartments, as in complex with microtubules and actin cytoskeleton [50, 51] and in the nucleus, where interaction with c-Jun and β-CATENIN followed by formation of the stable β-CATENIN/TCF complex was also demonstrated [>>52<<–54].
n3:mentions: n2:7720076 n2:15720724 n2:20006983

Subject Item: _:vb46893606
rdf:type: n4:Section
dc:title: materials and methods
n4:contains: _:vb46893608 _:vb46893609 _:vb46893610 _:vb46893607

Subject Item: _:vb46893607
rdf:type: n3:Context
rdf:value: Ponceau method to immunoblot was used to ensure equal protein loading [>>97<<]. Proteins recognized by antibodies were revealed by ECL technique, following the instructions of the manufacturer (Amersham Biosciences, Piscataway, NJ).
n3:mentions: n2:2429581

Subject Item: _:vb46893608
rdf:type: n3:Context
rdf:value: Nuclear extracts of each hippocampus from 4-, 12- and 24-month-old animals were prepared as previously described [>>98<<]. Briefly, hippocampal structures were homogenized using a Dounce homogenizer in cold PBS supplemented with 0.5 mM PMSF, 2.5 μg/ml leupeptin and 2.5 μg/ml antipain, and centrifuged at 4°C for 30 sec at 12,000×g.
n3:mentions: n2:8764593

Subject Item: _:vb46893609
rdf:type: n3:Context
rdf:value: The resulting supernatants containing nuclear proteins were stored at −80°C. Protein concentration was determined using the Bio-Rad colorimetric assay [>>99<<].
n3:mentions: n2:942051

Subject Item: _:vb46893610
rdf:type: n3:Context
rdf:value: EMSA for NF-κB was performed by using the gel shift assay kit from Promega (Madison, WI), as described previously [>>98<<]. 32P-NF-κB double-stranded consensus oligonucleotide probe (5′-AGTTGAGGGGACTTTCC CAGGC-3′; 25,000 cpm) and nuclear extracts (15 μg) were used.
n3:mentions: n2:8764593

Subject Item: _:vb46893611
rdf:type: n4:Section
dc:title: results
n4:contains: _:vb46893612 _:vb46893613 _:vb46893614 _:vb46893615 _:vb46893616

Subject Item: _:vb46893612
rdf:type: n3:Context
rdf:value: Once GSK-3β could be considered as a potential therapeutic target for diabetes and neurological disorders due to its role in insulin pathway substrates and inflammation process [>>55<<, 56], western blot assays were performed to verify the presence of some age related changes in AKT and GSK-3β activity.
n3:mentions: n2:21736545

Subject Item: _:vb46893613
rdf:type: n3:Context
rdf:value: Once GSK-3β could be considered as a potential therapeutic target for diabetes and neurological disorders due to its role in insulin pathway substrates and inflammation process [55, >>56<<], western blot assays were performed to verify the presence of some age related changes in AKT and GSK-3β activity.
n3:mentions: n2:24642411

Subject Item: _:vb46893614
rdf:type: n3:Context
rdf:value: WNT activation does not lead to Ser9 phosphorylation, there is a pool of GSK-3β that is present in a large protein complex, called destruction complex, which includes, in addition to β-CATENIN and GSK-3β, the proteins DVL, AXIN and CK1 [>>42<<]. Furthermore, WNT/β-CATENIN signaling can induce the transcription of Axin2 gene, which completes a negative feedback acting as a negative regulator of the signaling pathway [57].
n3:mentions: n2:22952392

Subject Item: _:vb46893615
rdf:type: n3:Context
rdf:value: Furthermore, WNT/β-CATENIN signaling can induce the transcription of Axin2 gene, which completes a negative feedback acting as a negative regulator of the signaling pathway [>>57<<].
n3:mentions: n2:11809808

Subject Item: _:vb46893616
rdf:type: n3:Context
rdf:value: status and decrease of DVL-2 linked to β-CATENIN pathway in hippocampus, microglia should become activated and high levels of glutamate (GLU) is frequently associated with impaired handling of extracellular GLU by gliotic astrocyte [>>100<<–103].
n3:mentions: n2:23320155 n2:16944320 n2:17497670

Subject Item: _:vb46893617
rdf:type: n4:Section
dc:title: discussion
n4:contains: _:vb46893618 _:vb46893619 _:vb46893620 _:vb46893621 _:vb46893622 _:vb46893623 _:vb46893624 _:vb46893625 _:vb46893626 _:vb46893627 _:vb46893628 _:vb46893629 _:vb46893630 _:vb46893631 _:vb46893632 _:vb46893633 _:vb46893634 _:vb46893635 _:vb46893636 _:vb46893637 _:vb46893638 _:vb46893639 _:vb46893640 _:vb46893641 _:vb46893642 _:vb46893643 _:vb46893644 _:vb46893645 _:vb46893646 _:vb46893647 _:vb46893648 _:vb46893649 _:vb46893650 _:vb46893651 _:vb46893652 _:vb46893653 _:vb46893654 _:vb46893655 _:vb46893656

Subject Item: _:vb46893618
rdf:type: n3:Context
rdf:value: that likely plays an important role in neuroinflammatory response; while the homodimer p50/p50 is well known as a stimulus-specific repressor of gene activation, relevant to modulate the activation of inflammatory response genes [>>58<<].
n3:mentions: n2:17693123

Subject Item: _:vb46893619
rdf:type: n3:Context
rdf:value: The result presented here is in agreement with previous data which showed an increase of NF-кB activity in a variety of tissues along aging, such as hypothalamus [>>59<<], frontal cortex, cerebellum [60], as well as in liver of 30-month-old rats [61].
n3:mentions: n2:23636330

Subject Item: _:vb46893620
rdf:type: n3:Context
rdf:value: The result presented here is in agreement with previous data which showed an increase of NF-кB activity in a variety of tissues along aging, such as hypothalamus [59], frontal cortex, cerebellum [>>60<<], as well as in liver of 30-month-old rats [61].
n3:mentions: n2:9143018

Subject Item: _:vb46893621
rdf:type: n3:Context
rdf:value: presented here is in agreement with previous data which showed an increase of NF-кB activity in a variety of tissues along aging, such as hypothalamus [59], frontal cortex, cerebellum [60], as well as in liver of 30-month-old rats [>>61<<]. In addition, inhibition of NF-кB activity seems to lead to a delayed onset of age-related symptoms and pathologies in animal models, and it has been linked with known lifespan regulators [14, 62].
n3:mentions: n2:14766800

Subject Item: _:vb46893622
rdf:type: n3:Context
rdf:value: In addition, inhibition of NF-кB activity seems to lead to a delayed onset of age-related symptoms and pathologies in animal models, and it has been linked with known lifespan regulators [>>14<<, 62]. Therefore, the importance of NF-кB signaling has been very well described in inflammaging and its activators could be potential aging biomarkers [63, 64].
n3:mentions: n2:21483034

Subject Item: _:vb46893623
rdf:type: n3:Context
rdf:value: In addition, inhibition of NF-кB activity seems to lead to a delayed onset of age-related symptoms and pathologies in animal models, and it has been linked with known lifespan regulators [14, >>62<<]. Therefore, the importance of NF-кB signaling has been very well described in inflammaging and its activators could be potential aging biomarkers [63, 64].
n3:mentions: n2:22396894

Subject Item: _:vb46893624
rdf:type: n3:Context
rdf:value: Therefore, the importance of NF-кB signaling has been very well described in inflammaging and its activators could be potential aging biomarkers [>>63<<, 64].
n3:mentions: n2:17964225

Subject Item: _:vb46893625
rdf:type: n3:Context
rdf:value: Moreover, we found an age-related increase of TNF-α levels, a cytokine that plays a central role in the onset and maintenance of inflammation [>>65<<], and a decrease of IL-10 levels, a prototypical anti-inflammatory cytokine [66, 67], in rat hippocampus (Fig.
n3:mentions: n2:9605921

Subject Item: _:vb46893626
rdf:type: n3:Context
rdf:value: Moreover, we found an age-related increase of TNF-α levels, a cytokine that plays a central role in the onset and maintenance of inflammation [65], and a decrease of IL-10 levels, a prototypical anti-inflammatory cytokine [>>66<<, 67], in rat hippocampus (Fig. 2). The increase in the ratio TNF-α/IL-10 might be related with the age-related maintenance of NF-кB activation, although the participation of other pathways cannot be ruled out.
n3:mentions: n2:11244051

Subject Item: _:vb46893627
rdf:type: n3:Context
rdf:value: Moreover, we found an age-related increase of TNF-α levels, a cytokine that plays a central role in the onset and maintenance of inflammation [65], and a decrease of IL-10 levels, a prototypical anti-inflammatory cytokine [66, >>67<<], in rat hippocampus (Fig. 2). The increase in the ratio TNF-α/IL-10 might be related with the age-related maintenance of NF-кB activation, although the participation of other pathways cannot be ruled out.
n3:mentions: n2:11942558

Subject Item: _:vb46893628
rdf:type: n3:Context
rdf:value: However, in some circumstances as chronic inflammatory process observed in aging, GCs can enhance instead of reducing inflammation [>>68<<], which could justify the increased levels of TNF-α observed and the reduction of IL-10.
n3:mentions: n2:19840546

Subject Item: _:vb46893629
rdf:type: n3:Context
rdf:value: Short-term GCs, as with immune activation, can be beneficial, whereas long-term GCs and prolonged or exaggerated inflammation may result in adverse consequences [>>69<<].
n3:mentions: n2:18650913

Subject Item: _:vb46893630
rdf:type: n3:Context
rdf:value: In fact, recent data from our laboratory have shown that nephrectomy-induced cognitive impairment in rats seems to be related to an increase in GCs levels in cerebrospinal fluid (CSF) and TNF-α/IL-10 ratio compared to the Sham group [>>70<<]. Furthermore, chronic unpredictable stress (CUS) potentiated lipo-polysaccharide (LPS)-induced NF-кB activation and pro-inflammatory cytokine expression in the frontal cortex and hippocampus, but not in hypothalamus of rats.
n3:mentions: n2:25961830

Subject Item: _:vb46893631
rdf:type: n3:Context
rdf:value: The pro-inflammatory effects of stress were mediated by GC receptors since pretreatment with the GR antagonist RU-486 reverted the stress effects on NF-кB potentiation [>>25<<].
n3:mentions: n2:16597735

Subject Item: _:vb46893632
rdf:type: n3:Context
rdf:value: dampening inflammation in some circumstances where inflammatory stimulus is weak, whilst enhancing inflammation in other circumstances, at least in part via the sensitization of microglia reactivity, increasing glutamate (GLU) release [>>71<<] which in turn can induce NF-кB activation [72].
n3:mentions: n2:17678955

Subject Item: _:vb46893633
rdf:type: n3:Context
rdf:value: inflammatory stimulus is weak, whilst enhancing inflammation in other circumstances, at least in part via the sensitization of microglia reactivity, increasing glutamate (GLU) release [71] which in turn can induce NF-кB activation [>>72<<].
n3:mentions: n2:14614955

Subject Item: _:vb46893634
rdf:type: n3:Context
rdf:value: Another hallmark of aging that seems to be one of the most promising therapeutic strategy for neurodegenerative disorders until this moment is the mechanistic target of rapamycin (mTOR) [1, >>73<<]. Moreover, AKT is a well-known component of the mTOR signaling pathway [74], that together with WNT signaling can prevent caspase activation and apoptosis [75].
n3:mentions: n2:25341517

Subject Item: _:vb46893635
rdf:type: n3:Context
rdf:value: Moreover, AKT is a well-known component of the mTOR signaling pathway [>>74<<], that together with WNT signaling can prevent caspase activation and apoptosis [75].
n3:mentions: n2:26328016

Subject Item: _:vb46893636
rdf:type: n3:Context
rdf:value: Moreover, AKT is a well-known component of the mTOR signaling pathway [74], that together with WNT signaling can prevent caspase activation and apoptosis [>>75<<]. However during the aging process mTOR signaling is reduced, as well as AKT [45], and WNT/β-CATENIN in hippocampus, as suggested in this manuscript and by other groups, in hippocampal neurons [76] and in human fibroblast cell lineage
n3:mentions: n2:22388478

Subject Item: _:vb46893637
rdf:type: n3:Context
rdf:value: However during the aging process mTOR signaling is reduced, as well as AKT [>>45<<], and WNT/β-CATENIN in hippocampus, as suggested in this manuscript and by other groups, in hippocampal neurons [76] and in human fibroblast cell lineage [77].
n3:mentions: n2:25789082

Subject Item: _:vb46893638
rdf:type: n3:Context
rdf:value: However during the aging process mTOR signaling is reduced, as well as AKT [45], and WNT/β-CATENIN in hippocampus, as suggested in this manuscript and by other groups, in hippocampal neurons [76] and in human fibroblast cell lineage [>>77<<].
n3:mentions: n2:17643369

Subject Item: _:vb46893639
rdf:type: n3:Context
rdf:value: Studies from literature have suggested that mis-regulation of canonical WNT signaling can be involved in Alzheimer’s disease (AD) [>>78<<, 79] due to the fact that AD patients that carries a mutation in presenilin-1 have very low levels of β-Catenin [80].
n3:mentions: n2:17143299

Subject Item: _:vb46893640
rdf:type: n3:Context
rdf:value: Studies from literature have suggested that mis-regulation of canonical WNT signaling can be involved in Alzheimer’s disease (AD) [78, >>79<<] due to the fact that AD patients that carries a mutation in presenilin-1 have very low levels of β-Catenin [80].
n3:mentions: n2:17517621

Subject Item: _:vb46893641
rdf:type: n3:Context
rdf:value: literature have suggested that mis-regulation of canonical WNT signaling can be involved in Alzheimer’s disease (AD) [78, 79] due to the fact that AD patients that carries a mutation in presenilin-1 have very low levels of β-Catenin [>>80<<]. An interesting information is that Insulin like growth factor-1 (IGF1) signaling that is mediated via the activation of PI3K and AKT signaling seems to be very important for dendritic growth [76] and to be regulated by WNT/ β-CATENIN
n3:mentions: n2:9790190

Subject Item: _:vb46893642
rdf:type: n3:Context
rdf:value: information is that Insulin like growth factor-1 (IGF1) signaling that is mediated via the activation of PI3K and AKT signaling seems to be very important for dendritic growth [76] and to be regulated by WNT/ β-CATENIN signaling [>>81<<]. In an elegant approach, Kim et al., have demonstrated that hippocampal neurons treated with 1μM ICG-001, a small molecule that selectively inhibits TCF/ β-CATENIN transcription [82], for 24 hours, has a decrease in AKT phosphorylation
n3:mentions: n2:12154096

Subject Item: _:vb46893643
rdf:type: n3:Context
rdf:value: In an elegant approach, Kim et al., have demonstrated that hippocampal neurons treated with 1μM ICG-001, a small molecule that selectively inhibits TCF/ β-CATENIN transcription [>>82<<], for 24 hours, has a decrease in AKT phosphorylation and an increase in neuronal degeneration [76].
n3:mentions: n2:15314234

Subject Item: _:vb46893644
rdf:type: n3:Context
rdf:value: In fact, GSK-3β has been linked to the modulation of an assembly of transcription factors, including the activation of NF-κB and inhibition of β-CATENIN [>>84<<].
n3:mentions: n2:22580404

Subject Item: _:vb46893645
rdf:type: n3:Context
rdf:value: 7), which is a product of the β-CATENIN signaling pathway and a negative feedback regulator of the pathway [>>44<<, 57]. Although there is some uncertainty about a functional cross-regulation between these two pathways (NF-кB and β-CATENIN) in hippocampus during aging process, it is well known that both pathways have shown complex roles for
n3:mentions: n2:11940574

Subject Item: _:vb46893646
rdf:type: n3:Context
rdf:value: 7), which is a product of the β-CATENIN signaling pathway and a negative feedback regulator of the pathway [44, >>57<<]. Although there is some uncertainty about a functional cross-regulation between these two pathways (NF-кB and β-CATENIN) in hippocampus during aging process, it is well known that both pathways have shown complex roles for pathogenesis
n3:mentions: n2:11809808

Subject Item: _:vb46893647
rdf:type: n3:Context
rdf:value: The Dishevelled family proteins (Dvls) are multifunctional intracellular proteins essential for the transduction of WNT signaling [>>86<<, 87]. DVL proteins are among the few signaling intermediaries common to both canonical and non-canonical pathways; however, it is only in the canonical one that DVL, in the presence of a WNT stimulus, is recruited to Fz receptor to form a
n3:mentions: n2:20006983

Subject Item: _:vb46893648
rdf:type: n3:Context
rdf:value: The Dishevelled family proteins (Dvls) are multifunctional intracellular proteins essential for the transduction of WNT signaling [86, >>87<<]. DVL proteins are among the few signaling intermediaries common to both canonical and non-canonical pathways; however, it is only in the canonical one that DVL, in the presence of a WNT stimulus, is recruited to Fz receptor to form a
n3:mentions: n2:23396967

Subject Item: _:vb46893649
rdf:type: n3:Context
rdf:value: non-canonical pathways; however, it is only in the canonical one that DVL, in the presence of a WNT stimulus, is recruited to Fz receptor to form a signalosome with AXIN and other proteins to inactivate β-CATENIN destruction complex [>>88<<, 89]. Otherwise, some studies have suggested that phosphorylation of DVL can occur in the absence of β-CATENIN stabilization [90] which would not be an appropriate measurement for our question.
n3:mentions: n2:17569865

Subject Item: _:vb46893650
rdf:type: n3:Context
rdf:value: pathways; however, it is only in the canonical one that DVL, in the presence of a WNT stimulus, is recruited to Fz receptor to form a signalosome with AXIN and other proteins to inactivate β-CATENIN destruction complex [88, >>89<<]. Otherwise, some studies have suggested that phosphorylation of DVL can occur in the absence of β-CATENIN stabilization [90] which would not be an appropriate measurement for our question.
n3:mentions: n2:21183076

Subject Item: _:vb46893651
rdf:type: n3:Context
rdf:value: Otherwise, some studies have suggested that phosphorylation of DVL can occur in the absence of β-CATENIN stabilization [>>90<<] which would not be an appropriate measurement for our question.
n3:mentions: n2:15143170

Subject Item: _:vb46893652
rdf:type: n3:Context
rdf:value: of β-CATENIN signaling pathway, which is in agreement with a very recent study that suggests physical exercise and environmental enrichment as factors that can attenuate the decrease in WNT signaling pathway along aging process [>>91<<].
n3:mentions: n2:24183784

Subject Item: _:vb46893653
rdf:type: n3:Context
rdf:value: as an important factor in normal functioning of the hippocampus [92] with growing evidence that its downregulation could be involved not only in cognitive decline associated with normal aging, but even with the physiology of AD [>>93<<]. Understanding the molecular mechanisms underlying this downregulation as well as strategies to reverse this decrease would be of fundamental importance.
n3:mentions: n2:25443287

Subject Item: _:vb46893654
rdf:type: n3:Context
rdf:value: studies have already suggested that strategies that induce neurogenesis and neuroprotection, such as exercise and reduced caloric intake, could be a potential mechanism to preserve and/or restore brain function during aging and injury [>>94<<], especially with respect to inflammatory process [95, 96].
n3:mentions: n2:17049865

Subject Item: _:vb46893655
rdf:type: n3:Context
rdf:value: neurogenesis and neuroprotection, such as exercise and reduced caloric intake, could be a potential mechanism to preserve and/or restore brain function during aging and injury [94], especially with respect to inflammatory process [>>95<<, 96].
n3:mentions: n2:24886300

Subject Item: _:vb46893656
rdf:type: n3:Context
rdf:value: neurogenesis and neuroprotection, such as exercise and reduced caloric intake, could be a potential mechanism to preserve and/or restore brain function during aging and injury [94], especially with respect to inflammatory process [95, >>96<<].
n3:mentions: n2:25818175

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