Role of BDNF Signaling in Memory Enhancement Induced by Transcranial Direct Current Stimulation

Cocco, Sara; Podda, Maria Vittoria; Grassi, Claudio

doi:10.3389/fnins.2018.00427

Cited by 34 publications

(20 citation statements)

References 78 publications

(93 reference statements)

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“…Alzheimer’s disease (AD) progression has also been associated with impaired reconsolidation and reduced BDNF signaling (Hock et al, 2000; Ohno, 2009), suggesting that increasing BDNF function during reconsolidation could partially counteract declarative memory deficits in AD patients. In this respect, transcranial direct current stimulation, which activates signaling downstream BDNF and elicits LTP-like mechanisms in rats, improves episodic and semantic memories in AD patients (Cocco et al, 2018) a result in line with earlier findings showing that the blood-brain barrier permeable TrkB agonist 7,8-dihydroxyflavone (7,8-DHF) ameliorates cognitive decline in AD animal models (Devi and Ohno, 2012).…”

Section: Implications Of Bdnf Signaling Manipulation During Memory Resupporting

confidence: 84%

On the Involvement of BDNF Signaling in Memory Reconsolidation

Gonzalez

Radiske

Cammarota

2019

Front. Cell. Neurosci.

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When retrieval occurs concomitantly with novelty detection, mismatch perception or reactivation of conflicting information, consolidated memories can enter into a labile state, and to persist, must be restabilized through a protein synthesis-dependent reconsolidation process during which their strength and content can be modified. Extensive literature implicates brain-derived neurotrophic factor (BDNF), a key regulator of synaptogenesis and synaptic plasticity, in the acquisition, consolidation and extinction of several memory types. However, the participation of BDNF in memory reconsolidation has been less studied. In this review, we discuss recent reports supporting the involvement of BDNF signaling in reactivation-induced memory updating.

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Section: Implications Of Bdnf Signaling Manipulation During Memory Resupporting

confidence: 84%

On the Involvement of BDNF Signaling in Memory Reconsolidation

Gonzalez

Radiske

Cammarota

2019

Front. Cell. Neurosci.

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“…It has also been hypothesized that molecular events underlying tDCS effects are initiated by increased Ca 2+ signaling via NMDAR and voltage-gated calcium channel activation (Pelletier and Cicchetti, 2014;Rohan et al, 2015). Indeed, Ca 2+dependent intracellular responses observed following tDCS include increased phosphorylation of CREB and CaMKII along with nitric oxide synthase activation (Kim et al, 2017;Cocco et al, 2018;Barbati et al, 2019). In keeping with these data, our Western immunoblot analyses showed enhanced pCREB Ser133 and pCaMKII Thr286 in tDCS-WT-3M mice.…”

Section: Discussionsupporting

confidence: 86%

“…Indeed, several studies, including our own, indicated that molecular determinants of plasticity and, particularly, the neurotrophin BDNF, are engaged and boosted by anodal tDCS, leading to enhanced plasticity and memory (Rohan et al, 2015;Podda et al, 2016;Kim et al, 2017;Cocco et al, 2018;Paciello et al, 2018;Stafford et al, 2018;Barbati et al, 2019;Kronberg et al, 2020).…”

Section: Discussionmentioning

confidence: 93%

Plasma BDNF Levels Following Transcranial Direct Current Stimulation Allow Prediction of Synaptic Plasticity and Memory Deficits in 3×Tg-AD Mice

Cocco

Rinaudo

Fusco

et al. 2020

Front. Cell Dev. Biol.

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Early diagnosis of Alzheimer's disease (AD) supposedly increases the effectiveness of therapeutic interventions. However, presently available diagnostic procedures are either invasive or require complex and expensive technologies, which cannot be applied at a larger scale to screen populations at risk of AD. We were looking for a biomarker allowing to unveil a dysfunction of molecular mechanisms, which underly synaptic plasticity and memory, before the AD phenotype is manifested and investigated the effects of transcranial direct current stimulation (tDCS) in 3×Tg-AD mice, an experimental model of AD which does not exhibit any long-term potentiation (LTP) and memory deficits at the age of 3 months (3×Tg-AD-3M). Our results demonstrated that tDCS differentially affected 3×Tg-AD-3M and age-matched wild-type (WT) mice. While tDCS increased LTP at CA3-CA1 synapses and memory in WT mice, it failed to elicit these effects in 3×Tg-AD-3M mice. Remarkably, 3×Tg-AD-3M mice did not show the tDCSdependent increases in pCREB Ser133 and pCaMKII Thr286 , which were found in WT mice. Of relevance, tDCS induced a significant increase of plasma BDNF levels in WT mice, which was not found in 3×Tg-AD-3M mice. Collectively, our results showed that plasticity mechanisms are resistant to tDCS effects in the pre-AD stage. In particular, the lack of BDNF responsiveness to tDCS in 3×Tg-AD-3M mice suggests that combining tDCS with dosages of plasma BDNF levels may provide an easy-to-detect and lowcost biomarker of covert impairment of synaptic plasticity mechanisms underlying memory, which could be clinically applicable. Testing proposed here might be useful to identify AD in its preclinical stage, allowing timely and, hopefully, more effective disease-modifying interventions.

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Section: Discussionmentioning

confidence: 99%

“…This is consistent with our findings of increased CREB5, CREB phosphorylation and cAMP accumulation by GLN in vivo and in vitro. Previous studies have noted the importance of BDNF/TrkB and CREB signaling in promoting cognition and memory formation [ 23 , 24 , 25 ]. The functioning of PDE4, which presumably reduces the cAMP levels, is significant for attenuating the PKA signaling, and thus the inhibitors for PDE4 have been a therapeutic option to treat different CNS diseases, including memory impairment [ 11 ].…”

Section: Discussionmentioning

confidence: 99%

Glucosamine Enhancement of BDNF Expression and Animal Cognitive Function

et al. 2020

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Brain-derived neurotrophic factor (BDNF) is an important factor for memory consolidation and cognitive function. Protein kinase A (PKA) signaling interacts significantly with BDNF-provoked downstream signaling. Glucosamine (GLN), a common dietary supplement, has been demonstrated to perform a variety of beneficial physiological functions. In the current study, an in vivo model of 7-week-old C57BL/6 mice receiving daily intraperitoneal injection of GLN (0, 3, 10 and 30 mg/animal) was subjected to the novel object recognition test in order to determine cognitive performance. GLN significantly increased cognitive function. In the hippocampus GLN elevated tissue cAMP concentrations and CREB phosphorylation, and upregulated the expression of BDNF, CREB5 and the BDNF receptor TrkB, but it reduced PDE4B expression. With the in vitro model in the HT22 hippocampal cell line, GLN exposure significantly increased protein and mRNA levels of BDNF and CREB5 and induced cAMP responsive element (CRE) reporter activity; the GLN-mediated BDNF expression and CRE reporter induction were suppressed by PKA inhibitor H89. Our current findings suggest that GLN can exert a cognition-enhancing function and this may act at least in part by upregulating the BDNF levels via a cAMP/PKA/CREB-dependent pathway.

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Role of BDNF Signaling in Memory Enhancement Induced by Transcranial Direct Current Stimulation

Cited by 34 publications

References 78 publications

On the Involvement of BDNF Signaling in Memory Reconsolidation

On the Involvement of BDNF Signaling in Memory Reconsolidation

Plasma BDNF Levels Following Transcranial Direct Current Stimulation Allow Prediction of Synaptic Plasticity and Memory Deficits in 3×Tg-AD Mice

Glucosamine Enhancement of BDNF Expression and Animal Cognitive Function

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