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Cell-Cell Interaction: A Technique To Improve The Function Of The Neural Cells

Correspondence to Author: Ashok Chakraborty, 

Ashok Chakraborty All Excel, Inc, CT,USA.


For Parkinson’s disease cell replacement therapy, dopaminergic neural cells can be employed (PD). When neural cell death in the brain causes a decrease in dopamine release, PD is the result. Therefore, it is thought that replacing neural cells in the brain from the outside may increase dopamine levels, which will help to reduce the symptoms of Parkinson’s disease. According to a recent analysis by Chakraborty and Diwan, neural stem cells (NSCs) are a better option than many other cells that can be considered for the same reasons. These hNSC cells also prevent any future dopamine-related issues, including as dyskinesia and motor neuron defects in the person, thanks to their mechanisms for maintaining the controlled level of dopamine. NSCs, however, senescence occurs after very sluggish growth few passes, hence it might not be possible to collect a large number of cells for the treatment of several PD patients. Here, we’ll talk about a potential way to alter cells to improve their capacity for dopamine production, growth, and survival. Cell-Cell interactions are frequently known to change the cells and can be taken into account for the aforementioned goal.

Keywords:Human Neural Stem Cells. Melanocytes. Cell-cell Interaction. Dopamine.Parkinson’s Disease

Introduction: Dopaminergic Parkinson’s disease (PD) is ultimately brought on by the death of neurons in the Substantia Nigra (SN) area of the brain [1,2]. The number of PD cases worldwide is significantly rising [3]. There are now no such curative treatments available, only some palliative ones such supplementing with DOPA, a precursor to dopamine [4]. Long-term DOPA supplement use, however, may result in dyskinesia, motor neuron damage, etc. [5]. The use of neural stem cells (NSCs), induced pluripotent stem cells (iPSCs), and other DOPA-producing cells including melanocytes as a cell therapy regiment for PD treatment has recently come under consideration [6,7]. However, hNSCs for PD cell treatment have been supported by a number of evidences in a recent study by Chakraborty and Diwan (2019) [8].In short, hNSCs can effectively regulate the physiologic level of that neurotransmitter since they are endowed with both Tyrosine hydroxylase, a critical rate-limiting enzyme for Dopamine synthesis, and its scavenging enzymes (DAT and MAO-B) [9]. As a result, cell therapy for Parkinson’s disease using human neural stem cells (hNSCs) should be preferable to levodopa therapy itself since it eliminates the risk of developing dyskinesia or a motor neuron deficiency in the long term. Additionally, hNSCs have the capacity to create glial-cell derived neural factors (GDNF) and brain-derived neural factors (BDNF), which can have an autocrine effect on hNSC development and dopamine production[10–12]. However, hNSCs have a poor rate of growth and enter senescence after a few passages, leaving little cell supply for therapeutic purposes [13].Mobility, endocrine control, heart health, and so forth. Dopamine serves as the main precursor of the sympathetic nervous system’s adrenaline neurotransmitter in the periphery, while noradrenaline serves as the adrenomedullary hormone. Tyrosine hydroxylase (TH) in dopamine-producing cells converts tyrosine to dihydroxyphenylalanine (DOPA), which is then decarboxylated to produce dopamine. Five different dopamine receptor types, D1 and D5, form couples with the Gs class of G proteins, which can stimulate cAMP formation, while D2, D3, and D4 form couples with the Gi class of G proteins, which can cause a decrease in intracellular cAMP formation [36, 37]. Additionally, TH is activated by cAMP [36, 37]. Dopamine, which is released by leukocytes and has both autocrine and paracrine immune modulatory effects. Forskolin, a cAMP inducer, has been shown to increase dopamine synthesis and storage in monocyte-derived dendritic cells (Mo-DCs) [38]. Dopamine also promotes T-cell differentiation to Th2 and increases cAMP levels in naive CD41 T cells via D1-receptors.DARPP32kDa, a dopamine- and cAMPregulated phosphoprotein, is phosphorylated at a higher level in the lesioned striatum in the hemi Parkinsonian rat model. DARPP-32, a key player in dopamine signalling, prevents PKA-targeted proteins from being dephosphorylated while sustaining D1DR-mediated signalling [39,40].

DiscussionMore than 200 different types of cells are thought to make up the human body. Specialized cells coordinate their behaviourthrough communication with other cells to form functional units including organs (brain, heart, liver, etc.), skin, bone, blood, and muscle. A single cell can connect with many other cells by physical contact, surface receptor-ligand interaction, cellular junctions, and secretory stimulation from nearby cells or those of distant organs. Cell-cell interaction is a complex process. Extensive research has been done on interactions involving factors that are secreted, such as growth factors and cytokines that are protein- or peptide-based, small molecules, and metabolites. Extracellular vesicle contacts have recently become another type of interaction. Additionally, the physiological surroundings of cells, including the extracellular matrix’s physical characteristics and its biochemical characteristics, such as oxygen levels (hypoxia) or nutrition, have an impact on how cells interact with one another (energy deprivation). Lipoxin (LX) biosynthesis is an illustration of LO-LO (lipoxygenases) interactions via transcellular circuits in people and other mammalian systems. Because LXs are a distinct type of local mediators made from arachidonic acid, they have unique and powerful biological functions [31]. Together, it seems that cell-cell interaction can support complicated biological processes in tissues, such as neurotransmission, embryonic development, wound healing, inflammation, etc., as well as coordinated cellular behaviour. Parkinson’s disease (PD) is a neurological condition that affects older adults and is characterised by tremor that appears gradually, delayed mobility, and cognitive decline. Parkinson’s disease is sporadic and has no known cause. Its molecular hallmarks include the death of neuronal cells in the subatantia nigra (SN) region of the brain. It is anticipated that a modified neural cells transplant in the brain will be a curative method.

ConclusionTogether, it appears that cell-cell interaction can enable coordinated cellular behaviour as well as complex biological processes in tissues like neurotransmission, embryonic development, wound healing, and inflammation. Parkinson’s disease (PD) is a neurological disorder that mostly affects older persons. It is characterised by gradual tremor development, delayed movement, and cognitive impairment. There is no known aetiology for Parkinson’s disease, which is sporadic. The death of neuronal cells in the subatantia nigra (SN) area of the brain is one of its chemical characteristics. A modified neural cell transplant in the brain is expected to be a curative procedure.

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Ashok Chakraborty. Cell-Cell Interaction: A Technique To Improve The Function Of The Neural Cells. Clinics of Neurology 2024.

Journal Info

  • Journal Name: Clinics of Neurology
  • Impact Factor: 2.1**
  • ISSN: 2836-256X
  • DOI: 10.52338/Conr
  • Short Name: CONR
  • Acceptance rate: 55%
  • Volume: 6 (2024)
  • Submission to acceptance: 25 days
  • Acceptance to publication: 10 days


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