Review Article - The Cognitive Neuroscience Journal (2022) Volume 5, Issue 4

Emotional memory and hippocampal-amygdala dynamism in context of Post-Traumatic Stress Disorder (PTSD).

Yun kai ^*

Department of Anesthesiology

*Corresponding Author:

Yun kai Department of Anesthesiology
Xi'an Jiaotong University
China
E-mail: Yun@qq.com

Received:26-Jul-2023, Manuscript No. AACNJ-23-109435; Editor assigned:28-Jul-2023, PreQC No. AACNJ-23-109435 (PQ); Reviewed:11-Aug-2023, QC No. AACNJ-23-109435; Revised:16- Aug-2023, Manuscript No. AACNJ-23-109435 (R); Published:23-Aug-2023, DOI:10.35841/ aacnj-6.4.157

Citation: kai Y. Unveiling the intricate connection: Neuroinflammation and neurodegenerative diseases. J Cogn Neurosci. 2023;6(4):157

Abstract

Proper communication between hippocampus and amygdala is essential in the formation of emotional memory. In Post-Traumatic Stress Disorder (PTSD) patients, the hippocampal-amygdala dynamism is compromised leading to various psychological and physical symptoms. Current methods of PTSD treatment carry a myopic vision by focus on alleviating specific symptoms alone limiting scope of treatment. The development of effective treatment methods for PTSD patients requires a holistic understanding of the role of hippocampus-amygdala complex by expanding on the current understanding of encoding, consolidation and retrieval of emotional memory.

Introduction

Neurodegenerative diseases, a group of debilitating conditions that progressively damage the nervous system, have long puzzled researchers and clinicians alike. Recent scientific advancements have revealed a compelling link between neuroinflammation and the pathogenesis of these disorders. Neuroinflammation, once considered a secondary response, is now recognized as a key player in the development and progression of various neurodegenerative diseases. This article delves into the complex interplay between neuroinflammation and neurodegeneration, shedding light on their intertwined relationship and its implications for novel therapeutic interventions [1].

Inflammation is a natural defense mechanism that the body employs to protect itself against harmful stimuli. Neuroinflammation is a specialized form of this process that occurs within the central nervous system (CNS) in response to injury, infection, toxins, or abnormal protein accumulation. Microglia, the immune cells of the brain, play a central role in neuroinflammation. While acute inflammation is a vital and protective response, chronic neuroinflammation can have detrimental effects on the CNS. Neuroinflammation is a hallmark of AD, with activated microglia and the release of pro-inflammatory molecules contributing to neuronal damage. Amyloid-beta plaques, a characteristic feature of AD, trigger an immune response that can exacerbate neuronal loss. In PD, neuroinflammation is closely linked to the loss of dopaminergic neurons. Chronic activation of microglia and the release of inflammatory cytokines contribute to neurodegeneration in the substantia nigra, a brain region involved in movement control. In ALS, neuroinflammation contributes to motor neuron degeneration. Immune cells infiltrate affected regions of the spinal cord, releasing factors that amplify inflammation and accelerate disease progression. Inflammation in HD is characterized by activated microglia and increased levels of inflammatory molecules. Neuroinflammation exacerbates the toxic effects of mutant huntingtin protein, leading to neuronal dysfunction. Inflammatory responses generate oxidative stress, causing damage to neurons and impairing cellular functions. This oxidative damage contributes to the accumulation of misfolded proteins and further exacerbates neurodegeneration [2].

Neuroinflammation can compromise the integrity of the BBB, allowing immune cells and molecules to infiltrate the brain. This immune system infiltration contributes to a self-perpetuating cycle of inflammation and neuronal damage. Dysregulated microglial responses can lead to a state of chronic activation, promoting neurotoxicity and impairing their beneficial roles in synaptic pruning and debris clearance. Targeting Neuroinflammation for Therapeutic Interventions The recognition of Neuroinflammation as a common feature in neurodegenerative diseases has sparked interest in developing therapies that modulate the inflammatory response. Drugs targeting specific inflammatory pathways or molecules are being explored to dampen neuroinflammation and its detrimental effects [3].

Modulating the activity of microglia and immune cells holds potential for regulating neuroinflammation and promoting neuroprotection. Neuroprotective Certain compounds have shown promise in suppressing neuroinflammatory responses and mitigating neurodegeneration. Given the role of oxidative stress, antioxidants could potentially counteract the damaging effects of inflammation-induced oxidative damage [4].

The intricate connection between Neuroinflammation and neurodegenerative diseases has reshaped our understanding of these complex disorders. As research continues to unveil the mechanisms underlying this relationship, it opens up new avenues for therapeutic interventions. Targeting neuroinflammation holds promise for slowing disease progression, protecting neurons, and ultimately improving the quality of life for individuals affected by neurodegenerative diseases. However, translating these discoveries into effective treatments requires further exploration, collaboration, and a comprehensive understanding of the delicate balance between immune responses and neural health [5].

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