Faculty Publications

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    Neuropathology of Neurological Disorders
    (Springer Nature, 2024) Andleeb Khan
    Neuropathology delineates the examination of cells and tissues, to assimilate the structure and function of the neurological system as well as the diagnosis and pathology of diseases that impact the nervous system. It studies the effects of disease on the nervous system and can be used to diagnose and categorize particular neurological conditions. This comprises studies of the muscles, nerves, and ganglia (the peripheral nervous system), and the brain and spinal cord (the central nervous system). A wide array of techniques such as immunohistochemistry, molecular biology, and light and electron microscopy are being used to observe neuropathological alterations in various neurological disorders. Neuropathology highlights the structural and functional observations of neurological diseases ranging from cellular to micro-anatomical constructs to identify the biomarkers that are responsible for the progression of the diseases. Several imaging technologies are also used which include CT scans and MRI to deeply examine the modifications in neurological disorders. The examination of several neurological disorders, such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and multiple sclerosis, rests severely on neuropathology. In this chapter, we will discuss about the neuropathology of several neurological disorders.
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    Mitochondrial Dysfunction and Its Role in Neurological Disorders
    (Springer Nature, 2024) Andleeb Khan
    Mitochondria, pivotal cell organelles recognized for their paramount role in cellular energy production, play a crucial part in neurological disorders such as Parkinson’s disease (PD), Alzheimer’s disease (AD), and multiple sclerosis when their functionality falters. Among the repercussions of mitochondrial dysfunction, neuroinflammation emerges as a prominent concern, eliciting an upsurge in the generation of reactive oxygen species (ROS). The deleterious effects of these ROS on nerve cells induce a cascade toward neurodegeneration. This chapter comprehensively delves into the adverse implications of mitochondrial dysfunction on the advancement of diverse neurological ailments, with particular emphasis on the pivotal role of neuroinflammation.
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    Current Understanding of DNA Methylation in the Pathogenesis of Neuropathic Pain
    (Springer Nature, 2024) Andleeb Khan
    Lesion or disease in the somatosensory nervous system is the root cause of neuropathic pain, which has a major negative influence on the quality of life. Injury to peripheral sensory nerves is well documented to change the expression of genes in the neurons and sensory nerves, which has a significant impact on the spinal cord’s synaptic plasticity and the onset and progression of chronic pain. N-methyl-D-aspartate (NMDA) receptors and α2δ1 are examples of pro-nociceptive genes, while potassium channels, opioid, and cannabinoid receptors are examples of anti-nociceptive genes. However, there is still more to learn about epigenetic mechanisms controlling the transcription of these genes. In this chapter, we explored the current research on the role of histone changes and DNA methylation in the development of neuropathic pain. We discussed the importance of neurotransmitter receptors and ion channels expressed transcriptionally under the regulation of these proteins in the dorsal root ganglia following nerve injury, which is frequently utilized in neuropathic pain models. A deeper understanding of the epigenetic reprogramming involved in the transition from acute to chronic pain may lead to the development of innovative neuropathic pain treatments.