Gamma rhythm low field magnetic stimulation alleviates neuropathologic changes and rescues memory and cognitive impairments in a mouse model of Alzheimer's disease

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Abstract

Introduction

The abnormal amyloid β (Aβ) accumulation and Aβ-related neural network dysfunction are considered central to the pathogenesis of Alzheimer's disease (AD) at the early stage. Deep-brain reachable low field magnetic stimulation (DMS), a novel noninvasive approach that was designed to intervene the network activity in brains, has been found to alleviate stress-related cognitive impairments.

Methods

Amyloid precursor protein/presenilin-1 transgenic mice (5XFAD) were treated with DMS, and cognitive behavior and AD-like pathologic changes in the neurochemical and electrophysiological properties in 5XFAD mice were assessed.

Results

We demonstrate that DMS treatment enhances cognitive performances, attenuates Aβ load, upregulates postsynaptic density protein 95 level, and promotes hippocampal long-term potentiation in 5XFAD mouse brain. Intriguingly, the gamma burst magnetic stimulation reverses the aberrant gamma oscillations in the transgenic hippocampal network.

Discussion

This work establishes a solid foundation for the effectiveness of DMS in treating AD and proposes a future study of gamma rhythm stimulation on reorganizing rhythmic neural activity in AD brain.

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Most cited references 33

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Learning induces long-term potentiation in the hippocampus.

Jonathan Whitlock, Arnold Heynen, Marshall G Hussain Shuler … (2006)

Years of intensive investigation have yielded a sophisticated understanding of long-term potentiation (LTP) induced in hippocampal area CA1 by high-frequency stimulation (HFS). These efforts have been motivated by the belief that similar synaptic modifications occur during memory formation, but it has never been shown that learning actually induces LTP in CA1. We found that one-trial inhibitory avoidance learning in rats produced the same changes in hippocampal glutamate receptors as induction of LTP with HFS and caused a spatially restricted increase in the amplitude of evoked synaptic transmission in CA1 in vivo. Because the learning-induced synaptic potentiation occluded HFS-induced LTP, we conclude that inhibitory avoidance training induces LTP in CA1.

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Record: found
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Long-term potentiation and memory.

M A Lynch (2004)

One of the most significant challenges in neuroscience is to identify the cellular and molecular processes that underlie learning and memory formation. The past decade has seen remarkable progress in understanding changes that accompany certain forms of acquisition and recall, particularly those forms which require activation of afferent pathways in the hippocampus. This progress can be attributed to a number of factors including well-characterized animal models, well-defined probes for analysis of cell signaling events and changes in gene transcription, and technology which has allowed gene knockout and overexpression in cells and animals. Of the several animal models used in identifying the changes which accompany plasticity in synaptic connections, long-term potentiation (LTP) has received most attention, and although it is not yet clear whether the changes that underlie maintenance of LTP also underlie memory consolidation, significant advances have been made in understanding cell signaling events that contribute to this form of synaptic plasticity. In this review, emphasis is focused on analysis of changes that occur after learning, especially spatial learning, and LTP and the value of assessing these changes in parallel is discussed. The effect of different stressors on spatial learning/memory and LTP is emphasized, and the review concludes with a brief analysis of the contribution of studies, in which transgenic animals were used, to the literature on memory/learning and LTP.

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Inflammation in neurodegenerative disease--a double-edged sword.

Tony Wyss-Coray, Lennart Mucke (2002)

Inflammation is a defense reaction against diverse insults, designed to remove noxious agents and to inhibit their detrimental effects. It consists of a dazzling array of molecular and cellular mechanisms and an intricate network of controls to keep them in check. In neurodegenerative diseases, inflammation may be triggered by the accumulation of proteins with abnormal conformations or by signals emanating from injured neurons. Given the multiple functions of many inflammatory factors, it has been difficult to pinpoint their roles in specific (patho)physiological situations. Studies of genetically modified mice and of molecular pathways in activated glia are beginning to shed light on this issue. Altered expression of different inflammatory factors can either promote or counteract neurodegenerative processes. Since many inflammatory responses are beneficial, directing and instructing the inflammatory machinery may be a better therapeutic objective than suppressing it.

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Author and article information

Contributors

Yan Zheng

Xiaomin Wang

Journal

Journal ID (nlm-ta): Alzheimers Dement (N Y)

Journal ID (iso-abbrev): Alzheimers Dement (N Y)

Title: Alzheimer's & Dementia : Translational Research & Clinical Interventions

Publisher: Elsevier

ISSN (Electronic): 2352-8737

Publication date PMC-release: 11 September 2017

Publication date Collection: November 2017

Publication date (Electronic): 11 September 2017

Volume: 3

Issue: 4

Pages: 487-497

Affiliations

[a ]Department of Neurobiology, Capital Medical University, Beijing, China

[b ]Key Laboratory for Neurodegenerative Disorders of the Ministry of Education, Capital Medical University, Beijing, China

[c ]Beijing Institute for Brain Disorders, Beijing, China

[d ]The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, China

[e ]Department of Neurobiology and State Key Laboratory of Proteomics, Beijing Institute of Basic Medical Sciences, Beijing, China

[f ]School of Electrical Engineering and Automation, Tianjin University, Tianjin, China

[g ]Department of Physiology, Capital Medical University, Beijing, China

Author notes

[∗ ]Corresponding author. Tel.: +86-10-83911829; Fax: +86-10-83911494. zhengyan@ 123456ccmu.edu.cn

[∗∗ ]Corresponding author. Tel.: +86-10-83911707; Fax: +86-10-63291984. xmwang@ 123456ccmu.edu.cn

[1]

These authors contributed equally to this work.

Article

Publisher ID: S2352-8737(17)30046-X

DOI: 10.1016/j.trci.2017.07.002

PMC ID: 5671620

PubMed ID: 29124106

SO-VID: 21503734-c7ef-4930-8bb5-240affbcd398

License:

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

Gamma rhythm low field magnetic stimulation alleviates neuropathologic changes and rescues memory and cognitive impairments in a mouse model of Alzheimer's disease

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Abstract

Introduction

Methods

Results

Discussion

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Alternative approaches to Alzheimer's Disease

Most cited references 33

Learning induces long-term potentiation in the hippocampus.

Long-term potentiation and memory.

Inflammation in neurodegenerative disease--a double-edged sword.

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