Neuroregenerative Plasticity in Health and Disease

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Molecular and Cellular Neuroscience".

Deadline for manuscript submissions: closed (31 August 2024) | Viewed by 57618

Special Issue Editor


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Guest Editor
Laboratory of Stem Cells and Neuroregeneration. Department of Animal Science, School of Life Sciences, Bharathidasan University, Tiruchirappalli 620024, Tamilnadu, India
Interests: neurogenesis; hippocampus; neuroplasticity

Special Issue Information

Dear Colleagues,

Obtaining insights into the molecular mechanisms underpinning the regulations of neuroplasticity responsible for learning and memory has been a highly significant scientific objective for the past few decades. The continual differentiation of neural stem cells into new neurons through the production of neuroblasts in the cognitive centers of the fully matured brain has been established as the cellular basis for neuroregenerative plasticity of learning and memory throughout life. The neurogenic process in the hippocampus denotes pattern separation, mood and cognition, which affects one’s health condition. Hippocampal neurogenesis can be positively modulated by many factors including an enriched environment, physical exercise, electro-compulsive stimulation, and supplementation with growth factors, neurotropic factors, and antioxidant and anti-depressant drugs. Although impaired neurogenesis results from the defective proliferative differentiation potential of neural stem cells (NSCs), the reduced survival and integration of newly generated neurons in the brain have recently been linked to the onset and progression of dementia in many neurocognitive, neuroimmune and metabolic disorders. Notably, Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), motor neuron diseases, neuroinflammation, stress, depression, anxiety, bipolar disorder, schizophrenia, gastrointestinal disorders, obesity, sleep disorders, metabolic disease, and an abnormal intake of food and antibiotics have been associated with aberrant neuroregenerative plasticity leading to emotional problems and dementia. Thus, therapeutic strategies that promote and sustain hippocampal neurogenesis have been considered to prevent aging and the disease-associated decline of memory.

Moreover, the occurrence of neurogenesis has been well established in the sub-ventricular zone (SVZ), hippocampus, rostral migratory stream (RMS)–olfactory bulb (OB) system, amygdala and hypothalamus of the brain in many adult organisms including humans. Upon cerebral stroke, the neural stem cells and neuroblasts in the SVZ appear to migrate to the infarct zone in the non-neurogenic areas such as the cortex and striatum, thereby indicating the spontaneous endogenous regenerative attempts of the brain. However, the fate determination of ectopically migrated neural stem cells and neuroblasts in the infarct zones needs to be further investigated for effective neural replacement therapy.

Over the past three decades, there has been enormous scientific progress made with regard to adult neurogenesis in experimental animals. However, the occurrence of neurogenesis in the adult human brain appears to be a longstanding scientific debate, while recent advancements in induced pluripotent stem cell technology provide advantages over the methodological disadvantages to assessing the neurogenic process. Recently, many infectious diseases including COVID-19 have also been identified to drastically alter the neurogenic process of the brain, leading to cognitive impairments. Therefore, the main goal of this Special Issue is to unveil the potential mechanisms underlying the regulation of neurogenesis in health and disease and decipher the potential signaling pathways and possible therapeutic targets to modulate the neurogenic process for the betterment of neurocognitive function in the elderly and subjects with disease conditions. Authors are welcome to submit original experimental research articles and review articles that cover the history, basic concepts, controversies, current research, clinical implications, technical advancements and roles of pro-neurogenic drugs, toxins and chemical detriments, as well as future perspectives related to the underlying biochemical, molecular and cellular mechanisms regulating adult neurogenesis and pharmacological and gene-editing strategies to treat dementia by mitigating aberrant hippocampal regenerative plasticity.

Submissions that use experimental evidence and potential mechanisms are encouraged, including topics such as: 1) aging, AD, PD, HD, ALS, ataxia, stroke, stress, anxiety and depression, as well as traumatic brain injury; 2) neuropsychiatric disorders including bipolar disease, schizophrenia and postpartum psychosis; 3) neuroimmune diseases; 4) abnormal circadian cycles, and endocrine, metabolic and malignant disorders; 5) gut homeostasis, dysbiosis and gastrointestinal disease; 6) infectious diseases including HIV, encephalitis, meningitis and COVID-19; 8) effects and impacts of physical exercise, enriched environments, nutraceuticals, probiotics, malnutrition antibiotics, and any other pharmacological agents in association with the regulation of adult neurogenesis and behavioral outcomes involving human tissues, live-imaging techniques, primary cultures, cell lines, induced pluripotent stem cells, animal models, and other relevant bioinformatics and mathematic methods.

Dr. Mahesh Kandasamy
Guest Editor

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Keywords

  • adult neurogenesis
  • dysbiosis
  • gut–brain axis
  • drugs
  • antioxidant
  • neurodegenerative disorders
  • dementia
  • COVID-19
  • behavior
  • cognitive functions

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Published Papers (5 papers)

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Research

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19 pages, 2651 KiB  
Article
Neuroimmune Support of Neuronal Regeneration and Neuroplasticity following Cerebral Ischemia in Juvenile Mice
by Ricaurte A. Marquez-Ortiz, Vesna Tesic, Daniel R. Hernandez, Bilkis Akhter, Nibedita Aich, Porter M. Boudreaux, Garrett A. Clemons, Celeste Yin-Chieh Wu, Hung Wen Lin and Krista M. Rodgers
Brain Sci. 2023, 13(9), 1337; https://doi.org/10.3390/brainsci13091337 - 17 Sep 2023
Cited by 4 | Viewed by 2148
Abstract
Ischemic damage to the brain and loss of neurons contribute to functional disabilities in many stroke survivors. Recovery of neuroplasticity is critical to restoration of function and improved quality of life. Stroke and neurological deficits occur in both adults and children, and yet [...] Read more.
Ischemic damage to the brain and loss of neurons contribute to functional disabilities in many stroke survivors. Recovery of neuroplasticity is critical to restoration of function and improved quality of life. Stroke and neurological deficits occur in both adults and children, and yet it is well documented that the developing brain has remarkable plasticity which promotes increased post-ischemic functional recovery compared with adults. However, the mechanisms underlying post-stroke recovery in the young brain have not been fully explored. We observed opposing responses to experimental cerebral ischemia in juvenile and adult mice, with substantial neural regeneration and enhanced neuroplasticity detected in the juvenile brain that was not found in adults. We demonstrate strikingly different stroke-induced neuroimmune responses that are deleterious in adults and protective in juveniles, supporting neural regeneration and plasticity. Understanding age-related differences in neuronal repair and regeneration, restoration of neural network function, and neuroimmune signaling in the stroke-injured brain may offer new insights for the development of novel therapeutic strategies for stroke rehabilitation. Full article
(This article belongs to the Special Issue Neuroregenerative Plasticity in Health and Disease)
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20 pages, 2615 KiB  
Article
A Mild Dose of Aspirin Promotes Hippocampal Neurogenesis and Working Memory in Experimental Ageing Mice
by Jemi Feiona Vergil Andrews, Divya Bharathi Selvaraj, Akshay Kumar, Syed Aasish Roshan, Muthuswamy Anusuyadevi and Mahesh Kandasamy
Brain Sci. 2023, 13(7), 1108; https://doi.org/10.3390/brainsci13071108 - 21 Jul 2023
Cited by 5 | Viewed by 3497
Abstract
Aspirin has been reported to prevent memory decline in the elderly population. Adult neurogenesis in the hippocampus has been recognized as an underlying basis of learning and memory. This study investigated the effect of aspirin on spatial memory in correlation with the regulation [...] Read more.
Aspirin has been reported to prevent memory decline in the elderly population. Adult neurogenesis in the hippocampus has been recognized as an underlying basis of learning and memory. This study investigated the effect of aspirin on spatial memory in correlation with the regulation of hippocampal neurogenesis and microglia in the brains of ageing experimental mice. Results from the novel object recognition (NOR) test, Morris water maze (MWM), and cued radial arm maze (cued RAM) revealed that aspirin treatment enhances working memory in experimental mice. Further, the co-immunohistochemical assessments on the brain sections indicated an increased number of doublecortin (DCX)-positive immature neurons and bromodeoxyuridine (BrdU)/neuronal nuclei (NeuN) double-positive newly generated neurons in the hippocampi of mice in the aspirin-treated group compared to the control group. Moreover, a reduced number of ionized calcium-binding adaptor molecule (Iba)-1-positive microglial cells was evident in the hippocampus of aspirin-treated animals. Recently, enhanced activity of acetylcholinesterase (AChE) in circulation has been identified as an indicative biomarker of dementia. The biochemical assessment in the blood of aspirin-treated mice showed decreased activity of AChE in comparison with that of the control group. Results from this study revealed that aspirin facilitates hippocampal neurogenesis which might be linked to enhanced working memory. Full article
(This article belongs to the Special Issue Neuroregenerative Plasticity in Health and Disease)
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Review

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31 pages, 925 KiB  
Review
The Cerebrovascular Side of Plasticity: Microvascular Architecture across Health and Neurodegenerative and Vascular Diseases
by Marialuisa Zedde and Rosario Pascarella
Brain Sci. 2024, 14(10), 983; https://doi.org/10.3390/brainsci14100983 - 28 Sep 2024
Cited by 5 | Viewed by 2250
Abstract
The delivery of nutrients to the brain is provided by a 600 km network of capillaries and microvessels. Indeed, the brain is highly energy demanding and, among a total amount of 100 billion neurons, each neuron is located just 10–20 μm from a [...] Read more.
The delivery of nutrients to the brain is provided by a 600 km network of capillaries and microvessels. Indeed, the brain is highly energy demanding and, among a total amount of 100 billion neurons, each neuron is located just 10–20 μm from a capillary. This vascular network also forms part of the blood–brain barrier (BBB), which maintains the brain’s stable environment by regulating chemical balance, immune cell transport, and blocking toxins. Typically, brain microvascular endothelial cells (BMECs) have low turnover, indicating a stable cerebrovascular structure. However, this structure can adapt significantly due to development, aging, injury, or disease. Temporary neural activity changes are managed by the expansion or contraction of arterioles and capillaries. Hypoxia leads to significant remodeling of the cerebrovascular architecture and pathological changes have been documented in aging and in vascular and neurodegenerative conditions. These changes often involve BMEC proliferation and the remodeling of capillary segments, often linked with local neuronal changes and cognitive function. Cerebrovascular plasticity, especially in arterioles, capillaries, and venules, varies over different time scales in development, health, aging, and diseases. Rapid changes in cerebral blood flow (CBF) occur within seconds due to increased neural activity. Prolonged changes in vascular structure, influenced by consistent environmental factors, take weeks. Development and aging bring changes over months to years, with aging-associated plasticity often improved by exercise. Injuries cause rapid damage but can be repaired over weeks to months, while neurodegenerative diseases cause slow, varied changes over months to years. In addition, if animal models may provide useful and dynamic in vivo information about vascular plasticity, humans are more complex to investigate and the hypothesis of glymphatic system together with Magnetic Resonance Imaging (MRI) techniques could provide useful clues in the future. Full article
(This article belongs to the Special Issue Neuroregenerative Plasticity in Health and Disease)
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16 pages, 1462 KiB  
Review
Physical Exercise and Mechanism Related to Alzheimer’s Disease: Is Gut–Brain Axis Involved?
by Javier Sanchez-Martinez, Patricio Solis-Urra, Jorge Olivares-Arancibia and Julio Plaza-Diaz
Brain Sci. 2024, 14(10), 974; https://doi.org/10.3390/brainsci14100974 - 27 Sep 2024
Cited by 1 | Viewed by 2901
Abstract
Background: Alzheimer’s disease is a progressive neurodegenerative disease characterized by structural changes in the brain, including hippocampal atrophy, cortical thinning, amyloid plaques, and tau tangles. Due to the aging of the global population, the burden of Alzheimer’s disease is expected to increase, making [...] Read more.
Background: Alzheimer’s disease is a progressive neurodegenerative disease characterized by structural changes in the brain, including hippocampal atrophy, cortical thinning, amyloid plaques, and tau tangles. Due to the aging of the global population, the burden of Alzheimer’s disease is expected to increase, making the exploration of non-pharmacological interventions, such as physical exercise, an urgent priority. Results: There is emerging evidence that regular physical exercise may mitigate the structural and functional declines associated with Alzheimer’s disease. The underlying mechanisms, however, remain poorly understood. Gut–brain axis research is a promising area for further investigation. This system involves bidirectional communication between the gut microbiome and the brain. According to recent studies, the gut microbiome may influence brain health through modulating neuroinflammation, producing neuroactive compounds, and altering metabolic processes. Exercise has been shown to alter the composition of the gut microbiome, potentially impacting brain structure and function. In this review, we aim to synthesize current research on the relationship between physical exercise, structural brain changes in Alzheimer’s disease, and the gut–brain axis. Conclusions: In this study, we will investigate whether changes in the gut microbiome induced by physical exercise can mediate its neuroprotective effects, offering new insights into the prevention and treatment of Alzheimer’s disease. By integrating findings from neuroimaging studies, clinical trials, and microbiome research, this review will highlight potential mechanisms. It will also identify key gaps in the literature. This will pave the way for future research directions. Full article
(This article belongs to the Special Issue Neuroregenerative Plasticity in Health and Disease)
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32 pages, 714 KiB  
Review
Exploring the Role of Neuroplasticity in Development, Aging, and Neurodegeneration
by Patrícia Marzola, Thayza Melzer, Eloisa Pavesi, Joana Gil-Mohapel and Patricia S. Brocardo
Brain Sci. 2023, 13(12), 1610; https://doi.org/10.3390/brainsci13121610 - 21 Nov 2023
Cited by 33 | Viewed by 45499
Abstract
Neuroplasticity refers to the ability of the brain to reorganize and modify its neural connections in response to environmental stimuli, experience, learning, injury, and disease processes. It encompasses a range of mechanisms, including changes in synaptic strength and connectivity, the formation of new [...] Read more.
Neuroplasticity refers to the ability of the brain to reorganize and modify its neural connections in response to environmental stimuli, experience, learning, injury, and disease processes. It encompasses a range of mechanisms, including changes in synaptic strength and connectivity, the formation of new synapses, alterations in the structure and function of neurons, and the generation of new neurons. Neuroplasticity plays a crucial role in developing and maintaining brain function, including learning and memory, as well as in recovery from brain injury and adaptation to environmental changes. In this review, we explore the vast potential of neuroplasticity in various aspects of brain function across the lifespan and in the context of disease. Changes in the aging brain and the significance of neuroplasticity in maintaining cognitive function later in life will also be reviewed. Finally, we will discuss common mechanisms associated with age-related neurodegenerative processes (including protein aggregation and accumulation, mitochondrial dysfunction, oxidative stress, and neuroinflammation) and how these processes can be mitigated, at least partially, by non-invasive and non-pharmacologic lifestyle interventions aimed at promoting and harnessing neuroplasticity. Full article
(This article belongs to the Special Issue Neuroregenerative Plasticity in Health and Disease)
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