Example Of Neuroplasticity Research Articles

Functional brain networks reorganization in the absence of medial temporal lobe structures: an example of neuroplasticity

AbstractBackgroundMedial temporal lobe structures are particularly vulnerable in age‐related neurodegenerative diseases. Here, we investigated the brain reorganization that allows maintaining relatively normal global cognitive functioning in patients with herpes simplex encephalitis (HSE) – an infectious neurological disease ‐ with marked focal atrophy most pronounced in the medial temporal lobes, particularly the hippocampus. Using rs‐fMRI we (i) characterized the patterns of functional network organization, and (ii) compared the intra‐/interhemispheric functional connectivity (FC) within each patient.MethodA total of nine HSE patients were included (see Table 1), four of them were affected mainly in the left (LH) and five in the right (RH) hemisphere. The rs‐fMRI data were acquired after a long‐term follow‐up (median 16 years) of the disease and were preprocessed using the AFNI software. For each patient, using different brain parcellations, we computed the intra‐ and inter‐FC strength for each hemisphere separately, yielding four measures of intra‐FC LH/RH and inter‐FC LH/RH . We grouped the subjects according to their lesion‐side and their performance (low, high) in a memory task.ResultWe observed, regardless of the lesion side, a highly variable pattern of disrupted FC in each patient. Left‐lesioned patients showed high intra‐FCLH/RH particularly in the precuneus/posterior cingulate (PPC) and the angular gyrus while right‐lesioned patients exhibited a high inter‐FCRH in the medial prefrontal cortex (MPFC) and PPC regions. Both left and right‐lesioned showed decreased intra‐FCLH/RH in ventral medial temporal areas, more pronounced in the left‐lesioned patients (Figure1). Right‐lesioned individuals who showed a pattern of inter‐FC within the right MPF and PPC performed consistently higher on the memory task (percentiles > 50) (Figure2).ConclusionThe substantial HSE‐induced medial temporal lobe lesions induce a global network reorganization. However, the side of the lesion seems to determine a specific pattern of network reorganization that is associated with differential cognitive performance. Left‐lesioned patients exhibited high PPC intra‐ and inter‐FCLH/RH and low memory performance while the right‐lesioned exhibited a high inter‐FCRH on the PPC and MPFC and better memory performance. Left lesions may result in nonadaptive brain reorganizations, however, right lesions, when linked to prefrontal brain reorganizations, may result in cognitive benefits and therefore be adaptive.

Radial stem astrocytes (aka neural stem cells): Identity, development, physio-pathology, and therapeutic potential.

Adult neurogenesis is a striking example of neuroplasticity, which enables adaptive network remodelling in response to all forms of environmental stimulation in physiological and pathological contexts. Dysregulation or cessation of adult neurogenesis contributes to neuropathology negatively affecting brain functions and hampering regeneration of the nervous tissue while targeting adult neurogenesis may provide the basis for potential therapeutic interventions. Neural stem cells in the adult mammalian brain are at the core and the entry point of adult neurogenesis. By their origin and properties, these cells belong to astroglia, and are represented by stem radial astrocytes (RSA) which exhibit multipotent "stemness". In the neurogenic niches, RSA interact with other cellular components, including protoplasmic astrocytes, which in turn regulate their neurogenic activity. In pathology, RSA become reactive, which affects their neurogenic capabilities, whereas reactive parenchymal astrocytes up-regulate stem cell hallmarks and are able to generate progeny that remain within astrocyte lineage. What makes RSA special is their multipotency, represented by self-renewing capacity capability to generate other cellular types as progeny. A broad understanding of the cellular features of RSA and parenchymal astrocytes provides an insight into the machinery that promotes/suppresses adult neurogenesis, clarifying principles of network remodelling. In this review, we discuss the cellular hallmarks, research tools, and models of RSA and astrocytes of the subventricular zone along the lateral ventricle and dentate gyrus of the hippocampus. We also discuss RSA in ageing, which has a great impact on the proliferative capacity of RSA, as well as the potential of RSA and astrocytes in therapeutic strategies aimed at cell replacement and regeneration.

Learning, Neurogenesis and Effects of Flavonoids on Learning.

Learning and memory are two of our mind's most magical abilities. Different brain regions have roles to process and store different types of memories. The hippocampus is the part of the brain responsible for receiving information and storing it in the neocortex. One of the most impressive characteristics of the hippocampus is its capacity for neurogenesis which is a process, new neurons are produced and then transformed into mature neurons and integrated into neural circuits. The neurogenesis process in the hippocampus, an example of neuroplasticity in the adult brain, is believed to aid hippocampal-dependent learning and memory. New neurons are constantly produced in the hippocampus and integrated into the pre-existing neuronal network, this allows old memories already stored in the neocortex to be removed from the hippocampus and replaced with new ones. Factors affecting neurogenesis in the hippocampus may also affect hippocampal-dependent learning and memory. The flavonoids can exert particularly powerful actions in mammalian cognition and improve hippocampaldependent learning and memory by positively affecting hippocampal neurogenesis.

Effect of Music Training on Auditory Brainstem and Middle Latency Responses

Purpose: The auditory system has potentials to reorganize its structure and function in response to environmental changes such as training, experience, learning, injury, and disease. This is called neuroplasticity. A typical example of neuroplasticity is the music training, which demands cognitive and neural challenges resulting in enhanced auditory perception. This study investigated the effect of music training on auditory evoked responses, particularly auditory brainstem and middle latency responses. Methods: Forty college students consisting of twenty students with music training (musicians) and twenty students without music training (non-musicians) participated in the study. All participants have normal ranges in terms of pure tone audiometry, speech audiometry, and tympanometry. Auditory brainstem response (ABR) and auditory middle latency response (AMLR) from both ears were tested. Absolute latencies and amplitudes of waves in ABR and AMLR were obtained and analyzed.Results: The absolute latencies of wave I and V significantly differed between musicians and non-musicians. They were shorter for musicians than for non-musicians. Significant differences were found in the interpeak latencies of wave III-V and I-V between musicians and non-musicians. They were also shorter in musicians than for non-musicians. In addition, there were only significant differences in the latency of Na in AMLR between musicians and non-musicians. It was shorter for a musician than for non-musician.Conclusion: ABR was more sensitive to the efficacy of the music training.

When the brain looks imperfect: An example of neuroplasticity as seen in a patient with arachnoid cysts – a case study

Objective: This study presents a case of a teenager (J.J.) prenatally diagnosed with large arachnoid cysts which did not allow parts of his brain to develop correctly. It aims to establish whether the congenital malformation affected the boy’s cognitive development.Method: In order to assess his cognitive development, the authors analyzed J.J.’s medical history, interviewed him and his parents and conducted neuropsychological examination.Results: Despite major parts of his brain undeveloped, the boy achieved average to outstanding scores in all tests.Conclusions: The scores achieved by J.J. suggest that normal development of cognitive abilities is possible even for a person whose central nervous system differs structurally from what is expected in a healthy subject.

Harnessing neuroplasticity for clinical applications

Neuroplasticity can be defined as the ability of the nervous system to respond to intrinsic or extrinsic stimuli by reorganizing its structure, function and connections. Major advances in the understanding of neuroplasticity have to date yielded few established interventions. To advance the translation of neuroplasticity research towards clinical applications, the National Institutes of Health Blueprint for Neuroscience Research sponsored a workshop in 2009. Basic and clinical researchers in disciplines from central nervous system injury/stroke, mental/addictive disorders, paediatric/developmental disorders and neurodegeneration/ageing identified cardinal examples of neuroplasticity, underlying mechanisms, therapeutic implications and common denominators. Promising therapies that may enhance training-induced cognitive and motor learning, such as brain stimulation and neuropharmacological interventions, were identified, along with questions of how best to use this body of information to reduce human disability. Improved understanding of adaptive mechanisms at every level, from molecules to synapses, to networks, to behaviour, can be gained from iterative collaborations between basic and clinical researchers. Lessons can be gleaned from studying fields related to plasticity, such as development, critical periods, learning and response to disease. Improved means of assessing neuroplasticity in humans, including biomarkers for predicting and monitoring treatment response, are needed. Neuroplasticity occurs with many variations, in many forms, and in many contexts. However, common themes in plasticity that emerge across diverse central nervous system conditions include experience dependence, time sensitivity and the importance of motivation and attention. Integration of information across disciplines should enhance opportunities for the translation of neuroplasticity and circuit retraining research into effective clinical therapies.

Mitochondria and neuroplasticity.

The production of neurons from neural progenitor cells, the growth of axons and dendrites and the formation and reorganization of synapses are examples of neuroplasticity. These processes are regulated by cell-autonomous and intercellular (paracrine and endocrine) programs that mediate responses of neural cells to environmental input. Mitochondria are highly mobile and move within and between subcellular compartments involved in neuroplasticity (synaptic terminals, dendrites, cell body and the axon). By generating energy (ATP and NAD+), and regulating subcellular Ca2+ and redox homoeostasis, mitochondria may play important roles in controlling fundamental processes in neuroplasticity, including neural differentiation, neurite outgrowth, neurotransmitter release and dendritic remodelling. Particularly intriguing is emerging data suggesting that mitochondria emit molecular signals (e.g. reactive oxygen species, proteins and lipid mediators) that can act locally or travel to distant targets including the nucleus. Disturbances in mitochondrial functions and signalling may play roles in impaired neuroplasticity and neuronal degeneration in Alzheimer's disease, Parkinson's disease, psychiatric disorders and stroke.

Decreased numbers of progenitor cells but no response to antidepressant drugs in the hippocampus of elderly depressed patients

Imaging studies have consistently documented hippocampal volume reductions in depression. Although depressive disorders are traditionally considered to have a neurochemical basis, recent studies suggest that impairments of structural plasticity contribute to the volume reductions and the related cognitive changes. This might result from repeated periods of stress that are a wellknown risk factor for depression. Adult neurogenesis is a prominent example of neuroplasticity that in rodents, is reduced by stress but stimulated by antidepressant drugs. Although reductions in neurogenesis have been proposed to contribute to the etiology of depression, only two studies have so far examined hippocampal cytogenesis in depression, but this was in a limited number of subjects with considerable interindividual variation, and these studies came to different conclusions. We therefore collected hippocampal tissue of 10 elderly control subject and 10 well-matched depressed patients that were highly comparable in terms of age, sex, pH-CSF and postmortem delay, and tested whether the numbers of MCM2-positive progenitors and PH3-positive proliferating cells were altered by depression or antidepressant treatment. A significant reduction was found in MCM2-, but not PH3-immunopositive cells in depression. Although this result is consistent with the concept that structural plasticity is decreased in depression, we could not confirm that antidepressant drugs had a stimulatory effect on these cells. This discrepancy may relate to anatomical differences, in medication, to neurogenesis-independent mechanisms of antidepressant action, or the age of the patients that was higher than in previous studies. Whether the reduction is a cause or consequence of depression awaits to be determined.

Neuroplasticity and psychiatry.

There is increasing concern that the course of psychiatric disorders may be affected by parameters such as the duration and intensity of symptoms of initial episodes of illness. As this indicates that abnormal function produces long-term changes within the brain, a review of the neuroscience literature regarding neuroplasticity is warranted. This article is a selective review, focusing in particular on results obtained from physiological experiments assessing plasticity within the mammalian neocortex. The possible relevance of results to psychiatry is discussed. While the most dramatic examples of neuroplasticity occur during a critical period of neural development, neuroplasticity can also occur in adult neocortex. Neuroplasticity appears to be activity-dependent: synaptic pathways that are intensively used may become strengthened, and conversely, there may be depression of transmission in infrequently used pathways. Results from neurophysiological experiments lend support to the clinical observation that the intensity and duration of a psychiatric disorder may adversely alter its long-term course. Rapid aggressive treatment may prevent this from occurring. While pharmacotherapy may reduce the duration and severity of symptoms, it may also have an independent, as yet unknown, effect on neuroplasticity.

Behavioral sensitization: characterization of enduring changes in rotational behavior produced by intermittent injections of amphetamine in male and female rats.

Factors influencing the behavioral sensitization ("reverse tolerance") produced by intermittent amphetamine (AMPH) injections were studied by quantifying rotational behavior in rats that had a unilateral 6-hydroxy-dopamine lesion of the substantia nigra. The results indicate that: a single injection of a low dose of AMPH enhances rotational behavior induced by a second injection of AMPH for up to 12 weeks; multiple, weekly injections of AMPH produce a progressive enhancement in rotational behavior, over-and-above that produced by a single injection; female rats show more robust sensitization than males following single or multiple injections of AMPH; this sex difference may be due to the suppression of sensitization by an androgen, because removal of testicular hormones potentiates sensitization; the long-lasting sensitization of rotational behavior produced by infrequent injections of AMPH is not due to drug-environment conditioning effects, but perhaps to a persistent AMPH-induced change(s) in brain catecholamine systems; and a simple change in DA receptors is probably not involved, because the sensitization produced by infrequent injections of AMPH does not influence the rotation produced by a subsequent injection of apomorphine. The results illustrate an intriguing example of neuroplasticity that may have clinical relevance.