The malleable brain: plasticity of neural circuits and behavior – a review from students to students

Schaefer, Natascha; Rotermund, Carola; Blumrich, Eva-Maria; Lourenco, Mychael V.; Joshi, Pooja; Hegemann, Regina U; Jamwal, Sumit; Ali, Nahid; Romero, Ezra Michelet García; Sharma, Saurabh; Ghosh, Shampa; Sinha, Jitendra Kumar; Loke, Hannah; Jain, Vishal; Lepeta, Katarzyna; Salamian, Ahmad; Sharma, Mahima; Golpich, Mojtaba; Nawrotek, Katarzyna; Paidi, Ramesh Kumar; Shahidzadeh, Sheila M.; Piermartiri, Tetsadê C. B.; Amini, Elham; Pastor, Verónica; Wilson, Yvette; Adeniyi, Philip Adeyemi; Datusalia, Ashok Kumar; Vafadari, Behnam; Saini, Vedangana; Suárez-Pozos, Edna; Kushwah, Neetu; Fontanet, Paula; Turner, Anthony J.

doi:10.1111/jnc.14107

Cited by 35 publications

(22 citation statements)

References 351 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We found that recombinant irisin stimulated the cAMP/PKA/CREB pathway in human cortical slices (Fig. 5a-c), a pathway that plays important roles in memory formation and has been found to be impaired in AD models 33-35 . Recombinant irisin further increased cAMP and pCREB in mouse hippocampal slices (Fig.…”

Section: Resultsmentioning

confidence: 86%

Exercise-linked FNDC5/irisin rescues synaptic plasticity and memory defects in Alzheimer’s models

Lourenco

Frozza

Freitas

et al. 2019

Nat Med

Self Cite

568

574

View full text Add to dashboard Cite

Defective brain hormonal signaling has been associated with Alzheimer’s disease (AD), a disorder characterized by synapse and memory failure. Irisin is an exercise-induced myokine released upon cleavage of membrane-bound precursor protein FNDC5, also expressed in the hippocampus. Here we show that FNDC5/irisin levels are reduced in AD hippocampi and cerebrospinal fluid, and in experimental AD models. Knockdown of brain FNDC5/irisin impaired long-term potentiation and novel object recognition memory in mice. Conversely, boosting brain levels of FNDC5/irisin rescued synaptic plasticity and memory in AD mouse models. Peripheral overexpression of FNDC5/irisin rescued memory impairment, whereas blockade of either peripheral or brain FNDC5/irisin attenuated the neuroprotective actions of physical exercise on synaptic plasticity and memory in AD mice. By showing that FNDC5/irisin is an important mediator of the beneficial effects of exercise in AD models, our findings place FNDC5/irisin as a novel agent capable of opposing synapse failure and memory impairment in AD.

show abstract

Section: Resultsmentioning

confidence: 86%

Exercise-linked FNDC5/irisin rescues synaptic plasticity and memory defects in Alzheimer’s models

Lourenco

Frozza

Freitas

et al. 2019

Nat Med

Self Cite

568

574

View full text Add to dashboard Cite

show abstract

“…Neurite deficits impair neural connectivity and alter brain function. Importantly, neurites are not fixed structures and are changeable to form the bases for neuroplasticity throughout lifespan . Neurites are regulated by many intrinsic genes and proteins including neurotrophins, membrane receptors, and voltage‐gated calcium channels as well as environmental factors .…”

Section: Introductionmentioning

confidence: 99%

Effects of antipsychotic drugs on neurites relevant to schizophrenia treatment

Huang

Song

2018

Medicinal Research Reviews

View full text Add to dashboard Cite

Although antipsychotic drugs are mainly used for treating schizophrenia, they are widely used for treating various psychiatric diseases in adults, the elderly, adolescents and even children. Today, about 1.2% of the worldwide population suffers from psychosis and related disorders, which translates to about 7.5 million subjects potentially targeted by antipsychotic drugs. Neurites project from the cell body of neurons and connect neurons to each other to form neural networks. Deficits in neurite outgrowth and integrity are implicated in psychiatric diseases including schizophrenia. Neurite deficits contribute to altered brain development, neural networking and connectivity as well as symptoms including psychosis and altered cognitive function. This review revealed that (1) antipsychotic drugs could have profound effects on neurites, synaptic spines and synapse, by which they may influence and regulate neural networking and plasticity; (2) antipsychotic drugs target not only neurotransmitter receptors but also intracellular signaling molecules regulating the signaling pathways responsible for neurite outgrowth and maintenance; (3) high doses and chronic administration of antipsychotic drugs may cause some loss of neurites, synaptic spines, or synapsis in the cortical structures. In addition, confounding effects causing neurite deficits may include elevated inflammatory cytokines and antipsychotic drug-induced metabolic side effects in patients on chronic antipsychotic therapy. Unraveling how antipsychotic drugs affect neurites and neural connectivity is essential for improving therapeutic outcomes and preventing aversive effects for patients on antipsychotic drug treatment.

show abstract

“…Human brains are susceptible to many things, and some events can result in their reprogramming, either positively or negatively, as underlined by Shaffer [50][51][52]. Amongst these events are the impacts of diseases and injuries on the nervous system, which are widely researched and documented.…”

Section: Brain Neural Network and Neuroplasticitymentioning

confidence: 99%

Achieving Neuroplasticity in Artificial Neural Networks through Smart Cities

Allam

2019

Smart Cities

View full text Add to dashboard Cite

Through the Internet of things (IoT), as promoted by smart cities, there is an emergence of big data accentuating the use of artificial intelligence through various components of urban planning, management, and design. One such system is that of artificial neural networks (ANNs), a component of machine learning that boasts similitude with brain neurological networks and its functioning. However, the development of ANN was done in singular fashion, whereby processes are rendered in sequence in a unidimensional perspective, contrasting with the functions of the brain to which ANN boasts similitude, and in particular to the concept of neuroplasticity which encourages unique complex interactions in self-learning fashion, thereby encouraging more inclusive urban processes and render urban coherence. This paper takes inspiration from Christopher Alexander’s Nature of Order and dwells in the concept of complexity theory; it also proposes a theoretical model of how ANN can be rendered with the same plastic properties as brain neurological networks with multidimensional interactivity in the context of smart cities through the use of big data and its emerging complex networks. By doing so, this model caters to the creation of stronger, richer, and more complex patterns that support Alexander’s concept of “wholeness” through the connection of overlapping networks. This paper is aimed toward engineers with interdisciplinary interest looking at creating more complex and intricate ANN models, and toward urban planners and urban theorists working on the emerging contemporary concept of smart cities.

show abstract

The malleable brain: plasticity of neural circuits and behavior – a review from students to students

Cited by 35 publications

References 351 publications

Exercise-linked FNDC5/irisin rescues synaptic plasticity and memory defects in Alzheimer’s models

Exercise-linked FNDC5/irisin rescues synaptic plasticity and memory defects in Alzheimer’s models

Effects of antipsychotic drugs on neurites relevant to schizophrenia treatment

Achieving Neuroplasticity in Artificial Neural Networks through Smart Cities

Contact Info

Product

Resources

About