Improved object recognition memory using post-encoding repetitive transcranial magnetic stimulation

Heath, Alesha; Brewer, M. Kathryn; Yesavage, Jerry; McNerney, M. Windy

doi:10.1016/j.brs.2021.11.009

Cited by 5 publications

(6 citation statements)

References 53 publications

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“…Our results showed that animals stimulated with iTBS had normal locomotor behavior and reduced anxiety levels, which was previously shown in animal models of epilepsy and post-traumatic stress disorder with the use of rTMS stimulation protocols ( Wang et al, 2015 , 2019 ). It has been suggested that rTMS induces neuronal plasticity, modulates neurotransmitter and neurotrophic factors leading to LTP-like changes in stimulated areas ( Uzair et al, 2022 ), thus improving cognitive processes ( Heath et al, 2021 ). Prolonged stimulation with iTBS could evoke similar mechanisms and alter neuronal excitability and levels of neurotrophic factors, thus improving cognitive status in the TMT model of neurodegeneration.…”

Section: Discussionmentioning

confidence: 99%

Intermittent Theta Burst Stimulation Ameliorates Cognitive Deficit and Attenuates Neuroinflammation via PI3K/Akt/mTOR Signaling Pathway in Alzheimer’s-Like Disease Model

Stekic

Zeljković

Kontic

et al. 2022

Front. Aging Neurosci.

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Neurodegeneration implies progressive neuronal loss and neuroinflammation further contributing to pathology progression. It is a feature of many neurological disorders, most common being Alzheimer’s disease (AD). Repetitive transcranial magnetic stimulation (rTMS) is a non-invasive stimulation which modulates excitability of stimulated brain areas through magnetic pulses. Numerous studies indicated beneficial effect of rTMS in several neurological diseases, including AD, however, exact mechanism are yet to be elucidated. We aimed to evaluate the effect of intermittent theta burst stimulation (iTBS), an rTMS paradigm, on behavioral, neurochemical and molecular level in trimethyltin (TMT)-induced Alzheimer’s-like disease model. TMT acts as a neurotoxic agent targeting hippocampus causing cognitive impairment and neuroinflammation, replicating behavioral and molecular aspects of AD. Male Wistar rats were divided into four experimental groups–controls, rats subjected to a single dose of TMT (8 mg/kg), TMT rats subjected to iTBS two times per day for 15 days and TMT sham group. After 3 weeks, we examined exploratory behavior and memory, histopathological and changes on molecular level. TMT-treated rats exhibited severe and cognitive deficit. iTBS-treated animals showed improved cognition. iTBS reduced TMT-induced inflammation and increased anti-inflammatory molecules. We examined PI3K/Akt/mTOR signaling pathway which is involved in regulation of apoptosis, cell growth and learning and memory. We found significant downregulation of phosphorylated forms of Akt and mTOR in TMT-intoxicated animals, which were reverted following iTBS stimulation. Application of iTBS produces beneficial effects on cognition in of rats with TMT-induced hippocampal neurodegeneration and that effect could be mediated via PI3K/Akt/mTOR signaling pathway, which could candidate this protocol as a potential therapeutic approach in neurodegenerative diseases such as AD.

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Section: Discussionmentioning

confidence: 99%

Intermittent Theta Burst Stimulation Ameliorates Cognitive Deficit and Attenuates Neuroinflammation via PI3K/Akt/mTOR Signaling Pathway in Alzheimer’s-Like Disease Model

Stekic

Zeljković

Kontic

et al. 2022

Front. Aging Neurosci.

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“…We explored the colocalization of SV2A, a marker of synaptic vesicles in the presynapse of both glutamatergic and GABAergic neurons with PSD95, a scaffolding protein in post-synapse of glutamatergic neurons. Colocalization of these puncta indicate active glutamatergic synapses in the CA1 [21]. rTMS stimulation to the cerebellum increased the colocalization of SV2A and PSD95 in the CA1 to 25.44% (±0.04), compared to 12.42% (±0.02) for the SHAM mice (Welch's t-test, p < 0.05; Figure 2A).…”

Section: Resultsmentioning

confidence: 98%

“…Given the sample size of n = 7 and n = 9 in each group, an expected effect size of 1.5 in the object recognition test, determined based on previous work [21], and p < 0.05, we were able to achieve a power of 0.79 for this preliminary analysis (G*Power 3.1, [22]). Data were first tested to confirm if they met assumptions of normality as assessed by examining the skewness, kurtosis and the Shapiro-Wilk value of the calculated residuals.…”

Section: Methodsmentioning

confidence: 92%

“…This current study also showed biochemical evidence that rTMS stimulation of the hindbrain altered hippocampal function. Unfortunately, we cannot distinguish with the experimental design if the increased synaptic connectivity of the hippocampus was due to direct alteration from the stimulation or due to the stimulation increasing the ability of the mice to perform the memory task, which then would induce greater hippocampal connections [21]. There is strong evidence to suggest a functional link between the hippocampus and cerebellum [3].…”

Section: Discussionmentioning

confidence: 99%

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Hindbrain Stimulation Modulates Object Recognition Discrimination Efficiency and Hippocampal Synaptic Connections

Heath,

Madore,

Diaz

et al. 2023

Brain Sciences

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(1) Background: The cerebellum is well known to have functionalities beyond the control of motor function. However, brain stimulation studies have not explored the potential of this region to impact downstream processes which are imperative to multiple neurological conditions. Our study aimed to look at preliminary evidence that hindbrain-targeted repetitive transcranial magnetic stimulation (rTMS) in mice could alter motor, cognitive and anxiety measures; (2) Methods: Male B6129SF2/J mice (n = 16) were given rTMS (n = 9) over lambda at 10 Hz for 10 min or Sham (n = 7) for 14 consecutive days. Mice then underwent a battery of behavioral measures. (3) Results: In the object recognition test, only rTMS-treated mice distinguished between the novel object at 5 min, whereas those that received Sham treatment continued to improve discrimination from 5 to 10 min. Additionally, over the 10 min test phase, rTMS-stimulated mice explored the objects less than the Sham mice. This was accompanied by increased colocalization of presynaptic and postsynaptic markers in the hippocampus in the rTMS mice (4) Conclusions: Hindbrain rTMS stimulation elicits improved processing speed in the object recognition test via structural plasticity mechanisms in the hippocampus and could provide additional ways of targeting these important substructures of the brain.

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“…This may be because the optimal rTMS parameters are undetermined [117] or because most rodent models administer rTMS while under restraint or anesthesia [118]. Newly developed methods demonstrate how to provide consistent rTMS to mice without restraint or anesthesia [119], and this method improved post-encoding memory in mice [120]. Indeed, rTMS in unrestrained triple transgenic Alzheimer's mice (3×TgAD) mice improved cholinergic and neurotrophic factor signaling, both of which are important for cognition and mTBI recovery [121].…”

Section: Rtms and Tdcs Benefits In Rodents After Tbimentioning

confidence: 99%

The Rehabilitation Potential of Neurostimulation for Mild Traumatic Brain Injury in Animal and Human Studies

McNerney,

Gurkoff,

Beard

et al. 2023

Brain Sciences

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Neurostimulation carries high therapeutic potential, accompanied by an excellent safety profile. In this review, we argue that an arena in which these tools could provide breakthrough benefits is traumatic brain injury (TBI). TBI is a major health problem worldwide, with the majority of cases identified as mild TBI (mTBI). MTBI is of concern because it is a modifiable risk factor for dementia. A major challenge in studying mTBI is its inherent heterogeneity across a large feature space (e.g., etiology, age of injury, sex, treatment, initial health status, etc.). Parallel lines of research in human and rodent mTBI can be collated to take advantage of the full suite of neuroscience tools, from neuroimaging (electroencephalography: EEG; functional magnetic resonance imaging: fMRI; diffusion tensor imaging: DTI) to biochemical assays. Despite these attractive components and the need for effective treatments, there are at least two major challenges to implementation. First, there is insufficient understanding of how neurostimulation alters neural mechanisms. Second, there is insufficient understanding of how mTBI alters neural function. The goal of this review is to assemble interrelated but disparate areas of research to identify important gaps in knowledge impeding the implementation of neurostimulation.

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Improved object recognition memory using post-encoding repetitive transcranial magnetic stimulation

Cited by 5 publications

References 53 publications

Intermittent Theta Burst Stimulation Ameliorates Cognitive Deficit and Attenuates Neuroinflammation via PI3K/Akt/mTOR Signaling Pathway in Alzheimer’s-Like Disease Model

Intermittent Theta Burst Stimulation Ameliorates Cognitive Deficit and Attenuates Neuroinflammation via PI3K/Akt/mTOR Signaling Pathway in Alzheimer’s-Like Disease Model

Hindbrain Stimulation Modulates Object Recognition Discrimination Efficiency and Hippocampal Synaptic Connections

The Rehabilitation Potential of Neurostimulation for Mild Traumatic Brain Injury in Animal and Human Studies

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