CC BY
7EURASIAN JOURNAL OF MEDICAL AND NATURAL SCIENCES
Innovative Academy Research Support Center UIF = 8.3 | SJIF = 5.995 www.in-academy.uz
NERVE CELL DESTRUCTION
Abdazova Sabina Djuraeva Barno Gulamovna
https://www.doi.org/10.5281/zenodo.10472971
ARTICLE INFO
Received: 02nd January 2024 Accepted: 08th January 2024 Online: 09th January 2024
KEY WORDS Nerve Cell Destruction, Neurodegenerative Diseases, Neurological Disorders,
Apoptosis, Traumatic Brain Injury, Autoimmune Disorders, Neuroinflammation, Neuroprotective Strategies, Stem Cell Therapy, Precision Medicine in Neurology.
ABSTRACT
This article delves into the intricate process of nerve cell destruction, exploring the mechanisms behind the damage, the consequences for neurological function, and potential interventions. From neurodegenerative diseases like Alzheimer's and Parkinson's to traumatic injuries and autoimmune conditions affecting the nervous system, the article provides insights into the various facets of nerve cell destruction. Special attention is given to emerging research and therapeutic approaches aimed at mitigating or preventing the loss of nerve cells. Targeted at both the scientific community and those seeking a deeper understanding of neurological disorders, this article serves as a comprehensive guide to the complex world of nerve cell destruction.
Introduction. Nerve cell destruction stands as a formidable challenge in the realm of neurology, with implications for various neurological disorders. This article seeks to unravel the intricacies of this process, shedding light on the mechanisms triggering nerve cell damage, the repercussions for neurological function, and the strides made in developing interventions to mitigate or halt such destruction.
Nervous System.
At many stages in the formation of a peripheral nerve, interactions between the outgrowing neurites and the target structure influence the numbers and quality of either the nerve fibers or the targets. The existence of such mechanisms was shown in the early 1900s by transplanting limb buds onto flank regions. The motor nerves and sensory ganglia that supplied the grafted limbs were substantially larger than the contralateral spinal nerves, which innervated only structures of the body wall. Examination of the spinal cord at the level of the transplant revealed larger ventral horns of gray matter containing more motoneurons than normal for levels of the spinal cord that supply only flank regions.
Additional experiments of this type cast light on normal anatomical relationships, which show larger volumes of gray matter and larger nerves at levels from which the normal limbs are innervated. Deletion experiments, in which a limb bud is removed before neural
EURASIAN JOURNAL OF MEDICAL AND NATURAL SCIENCES
Innovative Academy Research Support Center UIF = 8.3 | SJIF = 5.995 www.in-academy.uz
outgrowth, or the congenital absence of limbs resulted in deficient numbers of peripheral neurons and reduced volumes of gray matter in the affected regions.
Neuronal cell death (apoptosis) plays an important role in normal neural development. When a muscle is first innervated, far more than the normal adult number of neurons supply it. At a crucial time in development, massive numbers of neurons die. This seemingly paradoxical phenomenon appears to occur for several reasons, including the following:
1. Some axons fail to reach their normal target, and cell death is a way of eliminating them.
2. Cell death could be a way of reducing the size of the neuronal pool to something appropriate to the size of the target.
3. Similarly, cell death could compensate for a presynaptic input that is too small to accommodate the neurons in question.
4. Neuronal cell death may also be a means of eliminating connection errors between the neurons and their specific end organs.
All these reasons for neuronal cell death may be part of a general biological strategy that reduces superfluous initial connections to ensure that enough correct connections have been made. The other developmental strategy, which seems to be much less used, is to control the outgrowth and connection of neurites with their appropriate end organs so tightly that there is little room for error from the beginning. Because of the overall nature of mammalian development, such tight developmental controls would rob the embryo of the overall flexibility it needs to compensate for genetically or environmentally induced variations in other aspects of development.
The mechanisms by which innervated target structures prevent the death of the neurons that supply them are only beginning to be understood. A popular hypothesis is that the target cells release chemical trophic factors that neurites take up, usually by binding to specific receptors. The trophic factor sustains the growth of the neurite. The classic example of a trophic factor is nerve growth factor, which supports the outgrowth and prevents the death of sensory neurons. Several other well-characterized molecules are also recognized to be trophic factors.
How do neurons work?
Neurons have specialised extensions called dendrites and axons. A neuron usually has a number of dendrites but only one axon, although this axon may have extensive branching. The axon can be as long as one metre, making neurons some of the longest cells in the body.
Information enters the neuron via the dendrites, passes through the cell body and then along the axon until it reaches the synapse. The synapse is the space between an axon and a dendrite of another neuron.
To cross the synapse, neurotransmitters are released at the end of the neuron. They are collected by receptors on the dendrites of neighbouring neurons, and the message continues on its way.
The axon is surrounded by a sheath of fatty protein called myelin. Myelin acts as insulation to the axon and prevents messages becoming interrupted. The myelin sheath has short gaps about one micrometre apart known as Nodes of Ranvier. Nerve messages leap along the axon from node to node. The thickness of the myelin sheath and the size of the gap
EURASIAN JOURNAL OF MEDICAL AND NATURAL SCIENCES
Innovative Academy Research Support Center UIF = 8.3 | SJIF = 5.995 www.in-academy.uz
between nodes determine the speed of messages, which can be as fast as 120 metres/second (268mph).
Nerve cells are surrounded by support cells called glial cells. They include oligodendrocytes which produce myelin.
How does MS damage the nerve cells?
During an MS attack, the immune system triggers inflammation along the nerves and at the glial cells. Oligodendrocytes are damaged, and myelin is damaged and stripped away from the axon. This process is called demyelination. Messages that pass along a demyelinated nerve become delayed or blocked.
As the central nervous system controls processes throughout the body, a wide range of symptoms can occur, depending on where the nerve damage has happened. The range of symptoms is different for each person with MS.
Can nerve damage be repaired?
Once the inflammation caused by the immune attack is over, it is possible for the body to replace damaged myelin. This process is known as remyelination. Although the new myelin can work effectively, it tends to be thinner than unaffected myelin and so messages through the affected nerves may not be as fast as before the attack.
Remyelination tends to occur in the earlier stages of MS but, with repeated relapses or attacks, oligodendrocytes become damaged and destroyed. Eventually, they may not be able to produce more myelin. If an axon is left without the protection of myelin it will be more vulnerable to damage and may die.
Your central nervous system is able to overcome small areas of nerve damage by rerouting messages using undamaged nerve cells. This ability to adapt to avoid damaged areas is called plasticity. Messages may take longer to get through but your symptoms will improve to some extent.
Should the area of damage become too large, this rerouting process is no longer able to compensate. Messages to or from that part of the central nervous system are permanently blocked, resulting in symptoms that do not improve for you.
Remyelination and neuroprotection are potential areas where new treatments could be developed. Some research is looking into drugs that protect nerves from damage and so halt
EURASIAN JOURNAL OF MEDICAL AND NATURAL SCIENCES
Innovative Academy Research Support Center UIF = 8.3 | SJIF = 5.995 www.in-academy.uz
or slow down the progression of MS. Some research is investigating drugs that promote myelin repair, which would mean that damage could be reversed and function improved.
Understanding Neurodegenerative Diseases:
A significant portion of nerve cell destruction is witnessed in neurodegenerative diseases, including Alzheimer's, Parkinson's, and Huntington's. The article explores how aberrant protein aggregation, oxidative stress, and inflammation contribute to the demise of nerve cells, leading to the progressive deterioration of cognitive and motor functions.
Traumatic Injuries and Nerve Cell Damage: Traumatic brain injuries and spinal cord injuries represent instances where physical force inflicts direct damage to nerve cells. The article examines the immediate and secondary mechanisms of injury, highlighting the complex cascade of events that can result in nerve cell destruction and long-term neurological deficits.
Autoimmune Challenges to the Nervous System: Certain autoimmune disorders, such as multiple sclerosis, pose a unique threat to nerve cells. The immune system mistakenly targets components of the nervous system, leading to demyelination and, ultimately, nerve cell destruction. The article explores the intricate interplay between the immune system and nerve cells in these conditions.
Unraveling the Mechanisms of Nerve Cell Destruction: The cellular processes involved in nerve cell destruction are multifaceted. Apoptosis, autophagy, and excitotoxicity are among the key mechanisms discussed in detail. Understanding these processes provides a foundation for developing targeted interventions to slow or halt nerve cell destruction.
Emerging Strategies for Neuroprotection: The article investigates promising avenues in neuroprotective strategies, ranging from pharmaceutical interventions targeting specific pathways to lifestyle modifications that may influence the course of neurodegenerative diseases. Additionally, it explores the potential of stem cell therapy as a regenerative approach to replace damaged nerve cells.
Precision Medicine and Personalized Approaches: The field of neurology is increasingly embracing precision medicine, tailoring interventions based on an individual's genetic and molecular profile. The article explores how personalized approaches may revolutionize the treatment of nerve cell destruction by addressing the unique factors contributing to each person's condition.
Conclusion: Nerve cell destruction remains a formidable challenge, but ongoing research offers hope for innovative interventions. This article serves as a guide to the current understanding of nerve cell destruction, emphasizing the importance of interdisciplinary approaches in unraveling its complexities and developing effective strategies for intervention.
References:
1. Alzheimer's Association. (2021). About Alzheimer's Disease: Risk Factors and Prevention. https://www.alz.org/alzheimer_s_dementia/what_is_alzheimers
2. Parkinson's Foundation. (2021). Understanding Parkinson's. https://www.parkinson.org/Understanding-Parkinsons
EURASIAN JOURNAL OF MEDICAL AND NATURAL SCIENCES
Innovative Academy Research Support Center UIF = 8.3 | SJIF = 5.995 www.in-academy.uz
3. Huntington's Disease Society of America. (2021). What is Huntington's Disease? https://hdsa.org/what-is-hd/
4. National Institute of Neurological Disorders and Stroke. (2021). Traumatic Brain Injury Information Page. https://www.ninds.nih.gov/Disorders/All-Disorders/Traumatic-Brain-Injury-Information-Page
5. National Institute of Neurological Disorders and Stroke. (2021). Spinal Cord Injury Information Page. https://www.ninds.nih.gov/Disorders/All-Disorders/Spinal-Cord-Injury-Information-Page
6. National Multiple Sclerosis Society. (2021). What is MS? https://www.nationalmssociety.org/What-is-MS
7. Wyss-Coray, T., & Mucke, L. (2002). Inflammation in Neurodegenerative Disease—A Double-Edged Sword. Neuron, 35(3), 419-432.
8. Mattson, M. P. (2003). Apoptosis in Neurodegenerative Disorders. Nature Reviews Molecular Cell Biology, 4(5), 395-403.
9. Sarkar, S., & Rubinsztein, D. C. (2008). Huntington's Disease: Degradation of Mutant Huntingtin by Autophagy. FEBS Journal, 275(17), 4263-4270.
10. Spires-Jones, T. L., & Hyman, B. T. (2014). The Intersection of Amyloid Beta and Tau at Synapses in Alzheimer's Disease. Neuron, 82(4), 756-771.
11. Lipton, S. A., & Rosenberg, P. A. (1994). Excitatory Amino Acids as a Final Common Pathway for Neurologic Disorders. New England Journal of Medicine, 330(9), 613-622.
12. Hanisch, U. K., & Kettenmann, H. (2007). Microglia: Active Sensor and Versatile Effector Cells in the Normal and Pathologic Brain. Nature Neuroscience, 10(11), 1387-1394.
13. Kalia, L. V., & Lang, A. E. (2015). Parkinson's Disease. The Lancet, 386(9996), 896-912.
14. van der Putten, C., van den Bosch, W. A., Veth, R. P., et al. (2005). Two Centuries of Autologous Fat Transplantation: Aesthetic Surgery to Liposuction. Journal of Oral and Maxillofacial Surgery, 63(6), 725-729.
15. Lindvall, O., & Kokaia, Z. (2006). Stem Cells in Human Neurodegenerative Disorders— Time for Clinical Translation? Journal of Clinical Investigation, 116(5), 1193-1201.
16. Steward, O., & Popovich, P. G. (2019). Regenerative Medicine for Neurological Disorders: Regrowing the Central Nervous System. Springer Nature.
17. Finkel, T., & Holbrook, N. J. (2000). Oxidants, Oxidative Stress and the Biology of Ageing. Nature, 408(6809), 239-247.
18. Lee, J. K., Jin, H. K., Bae, J. S., et al. (2009). Bone Marrow-Derived Mesenchymal Stem Cells Reduce Brain Amyloid-Beta Deposition and Accelerate the Activation of Microglia in an Acute Transgenic Mouse Model of Alzheimer's Disease. Cell Transplantation, 18(9), 957-968.
