Low-frequency (1Hz) repetitive transcranial magnetic stimulation (rTMS) reverses Aβ1–42-mediated memory deficits in rats

Tan, Tao; Xie, Jiacun; Liu, Tiaotiao; Chen, Xiao‐Jia; Zheng, Xiaoyan; Tong, Zhiqian; Tian, Xin

doi:10.1016/j.exger.2013.05.001

Cited by 64 publications

(63 citation statements)

References 75 publications

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“…To the best of our knowledge, no other clinical non-invasive neuromodulation study has investigated the impact of a non-invasive brain stimulation treatment on the plasma levels of non-BDNF neurotrophic factors (Fidalgo et al, 2014). In fact, we were only able to identify one animal study that examined the effects of low-frequency rTMS on NGF hippocampal levels of rats (a NGF increase was observed after low-frequency rTMS) (Tan et al, 2013) and of high-frequency rTMS on GDNF expression levels in the substantia nigra pars compacta of rats subjected to an experimental model of Parkinson’s disease (also showing an increase of GDNF levels).…”

Section: Discussionmentioning

confidence: 99%

Assessment of non-BDNF neurotrophins and GDNF levels after depression treatment with sertraline and transcranial direct current stimulation in a factorial, randomized, sham-controlled trial (SELECT-TDCS): An exploratory analysis

Brunoni

Machado‐Vieira

Zarate

et al. 2015

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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The neurotrophic hypothesis of depression states that the major depressive episode is associated with lower neurotrophic factors levels, which increase with amelioration of depressive symptoms. However, this hypothesis has not been extended to investigate neurotrophic factors other than the brain-derived neurotrophic factor (BDNF). We therefore explored whether plasma levels of neurotrophins 3 (NT-3) and 4 (NT-4), nerve growth factor (NGF) and glial cell line derived neurotrophic factor (GDNF) changed after antidepressant treatment and correlated with treatment response. Seventy-three patients with moderate-to-severe, antidepressant-free unipolar depression were assigned to a pharmacological (sertraline) and a non-pharmacological (transcranial direct current stimulation, tDCS) intervention in a randomized, 2 × 2, placebo-controlled design. The plasma levels of NT-3, NT-4, NGF and GDNF were determined by enzyme-linked immunosorbent assay before and after a 6-week treatment course and analyzed according to clinical response and allocation group. We found that tDCS and sertraline (separately and combined) produced significant improvement in depressive symptoms. Plasma levels of all neurotrophic factors were similar across groups at baseline and remained significantly unchanged regardless of the intervention and of clinical response. Also, baseline plasma levels were not associated with clinical response. To conclude, in this 6-week placebo-controlled trial, NT-3, NT-4, NGF and GDNF plasma levels did not significantly change with sertraline or tDCS. These data suggest that these neurotrophic factors are not surrogate biomarkers of treatment response or involved in the antidepressant mechanisms of tDCS.

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Section: Discussionmentioning

confidence: 99%

Assessment of non-BDNF neurotrophins and GDNF levels after depression treatment with sertraline and transcranial direct current stimulation in a factorial, randomized, sham-controlled trial (SELECT-TDCS): An exploratory analysis

Brunoni

Machado‐Vieira

Zarate

et al. 2015

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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“…Tan et al, (2013) and Lee et al, (2013) reported that rTMS treatment can improve memory function. The former indicated that LF rTMS can reduce A␤ 1-42 -mediated memory deficit and the latter indicated that HF (10 Hz) rTMS had neuroprotective effect in a Parkinson's disease animal model.…”

Section: Discussionmentioning

confidence: 99%

“…rTMS has been used to treat neurological diseases, such as Alzheimer's disease, Parkinson's disease, epilepsy, depression and stroke (Guerra et al, 2011;Gross et al, 2007;Wu et al, 2008;Schönfeldt et al, 2010;Kwon et al, 2014;Carey et al, 2014). Tan et al (2013) reported that low frequency (LF) rTMS treatment not only improves spatial memory retrieval in normal rats, but also ameliorates A␤1-42-mediated memory deficits. Lee et al, (2013) indicated that the beneficial effect of rTMS treatment may be induced by upregulation of neurotrophic/growth factors in the Parkinson's disease animal model.…”

Section: Introductionmentioning

confidence: 99%

Functional protection of learning and memory abilities in rats with vascular dementia

Yang

Shi

Jin

et al. 2014

Restorative Neurology and Neuroscience

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Purpose: The present study clarified the effects of repetitive transcranial magnetic stimulation (rTMS) in rats with vascular dementia (VaD) and explored the underlying mechanisms. Methods: Two-vessel occlusion was used as a VaD model. Two weeks after carotid artery occlusion, high (5 Hz) or low (1 Hz) frequency rTMS were applied for 10 days. Spatial learning and memory abilities were tested with a Morris water maze. Hippocampal CA1 neurons were histologically examined. The expressions of mammalian target of rapamycin (mTOR) and eukaryotic initiation factor 4E (eIF-4E) in CA1 were detected by western blot, and immunohistochemistry. Results: Unlike unlesioned control animals, VaD rats had an impaired morphology of CA1 neurons and a reduced ability of spatial memory. rTMS significantly improved both, the morphology and the learning and memory abilities of VaD rats compared to untreated lesioned rats. Protein expressions of mTOR and eIF-4E in CA1 of VaD rats were lower than in control rats but rTMS significantly increased the expression compared to untreated VaD rats. Conclusions: rTMS promotes recovery of learning and memory abilities of VaD rats. Molecular analysis suggests that the beneficial effect of rTMS may be partly induced by upregulation of protein expressions of mTOR and eIF-4E in CA1.Keywords: Vascular dementia (VaD), repetitive transcranial magnetic stimulation (rTMS), learning and memory, mammalian target of rapamycin (mTOR), eukaryotic translation initiation factor 4 (eIF-4E), Morris Water Maze, 2-vessel occlusion 1 These authors contributed equally to this work.

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“…The levels of soluble Aβ were found to be increased in brains from AD patients and correlated highly with disease severity (Bateman et al 2012), and overaccumulation of Aβ in brains could result in the injury of neuronal cells (Tan et al 2013). Thus, reducing the toxicity of Aβ could be a therapeutic target for AD.…”

Section: Introductionmentioning

confidence: 98%

Cannabinoid Receptor CB1 Is Involved in Nicotine-Induced Protection Against Aβ1–42 Neurotoxicity in HT22 Cells

Jia

Lei

et al. 2014

J Mol Neurosci

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Emerging evidences suggest that nicotine exerts a neuroprotective effect on Alzheimer's disease (AD), yet the precise mechanism is not fully elucidated. Here, HT22 cells were exposed to amyloid beta protein fragment (Aβ)1-42 to mimic the pathological process of neuron in AD. We hypothesized that cannabinoid receptor CB1 is involved in the nicotine-induced neuroprotection against Aβ1-42 injury in HT22 cells. CB1 expression in HT22 cells was investigated by immunocytochemistry and Western blot. The injury of HT22 cells was evaluated by cellular morphology, cell viability, and lactate dehydrogenase (LDH) release. The apoptosis of HT22 cells was assessed by flow cytometry and expressions of Bcl-2 and Bax. The results demonstrated that nicotine markedly upregulated CB1 expression, increased cell viability, ameliorated cellular morphology, decreased LDH release, and reduced the apoptotic rate of HT22 cells exposed to Aβ1-42 for 24 h, while the blockade of CB1 or the inhibition of protein kinase C (PKC) partially reversed the neuroprotection. Furthermore, the blockade of CB1 reversed nicotine-induced PKC activation in HT22 cells exposed to Aβ1-42. These results suggest that CB1 is involved in the nicotine-induced neuroprotection against Aβ1-42 neurotoxicity, and the neuroprotection may be dependent on the activation of PKC.

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Low-frequency (1Hz) repetitive transcranial magnetic stimulation (rTMS) reverses Aβ1–42-mediated memory deficits in rats

Cited by 64 publications

References 75 publications

Assessment of non-BDNF neurotrophins and GDNF levels after depression treatment with sertraline and transcranial direct current stimulation in a factorial, randomized, sham-controlled trial (SELECT-TDCS): An exploratory analysis

Assessment of non-BDNF neurotrophins and GDNF levels after depression treatment with sertraline and transcranial direct current stimulation in a factorial, randomized, sham-controlled trial (SELECT-TDCS): An exploratory analysis

Functional protection of learning and memory abilities in rats with vascular dementia

Cannabinoid Receptor CB1 Is Involved in Nicotine-Induced Protection Against Aβ1–42 Neurotoxicity in HT22 Cells

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