Scholarlink

<p>Traumatic brain injury (TBI) and Alzheimer’s disease (AD), are two prominent neurological disorders. Both present a&#xa0;large number of clinical and socio-economic issues, but they are increasingly seen as having common pathways through which they cause disease. For both TBI and AD, oxidative stress and neuro-inflammatory responses lead to neuronal damages, impairment in synaptic function, and continued neuro-degeneration. After TBI, excessive production of oxygen and nitrogen free radicals damages mitochondrial function, while also activating microglial and astroglial cells chronically to cause inflammation. In patients with AD, continued oxidative damage leads to an accumulation of amyloid‑β protein and also leads to an increase in tau phosphorylation. There is an increasing body of literature demonstrating that the pathways by which TBI and AD occur may functionally connect short-term brain injuries to long-term neuro-degenerative processes. This article reviews the available data related to what currently drives the neuronal damage associated with TBI and AD through oxidative stress and inflammation and the available and generating treatment options—particularly antioxidants, anti-inflammatory agents, compounds protecting mitochondria, nanoparticles designed to deliver drugs, and phytochemicals with multi-targeted activity. The focus of this paper is on the scientific data supporting both the mechanistic pathways underlying the damage and the pharmacological/biological therapies that might treat the damage from a&#xa0;single point of view. The innovative aspect of this article lies in its demonstration of the relationship between oxidative stress and inflammation and its impact on the continuum of neuronal disease causing TBI leading to AD, and the potential of multi-targeted therapies to modify the ongoing disease processes.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Pathogenesis and treatment approaches for oxidative stress and neuroinflammation in traumatic brain injury and Alzheimer’s disease

  • 期刊论文

  • 发表日期：

    2025年12月1日

查看全文
  • Taru Mishra,
  • Shallu Sharma,
  • Sapna Joshi,
  • Shiv Kumar Prajapati,
  • Tejaswi

摘要

Traumatic brain injury (TBI) and Alzheimer’s disease (AD), are two prominent neurological disorders. Both present a large number of clinical and socio-economic issues, but they are increasingly seen as having common pathways through which they cause disease. For both TBI and AD, oxidative stress and neuro-inflammatory responses lead to neuronal damages, impairment in synaptic function, and continued neuro-degeneration. After TBI, excessive production of oxygen and nitrogen free radicals damages mitochondrial function, while also activating microglial and astroglial cells chronically to cause inflammation. In patients with AD, continued oxidative damage leads to an accumulation of amyloid‑β protein and also leads to an increase in tau phosphorylation. There is an increasing body of literature demonstrating that the pathways by which TBI and AD occur may functionally connect short-term brain injuries to long-term neuro-degenerative processes. This article reviews the available data related to what currently drives the neuronal damage associated with TBI and AD through oxidative stress and inflammation and the available and generating treatment options—particularly antioxidants, anti-inflammatory agents, compounds protecting mitochondria, nanoparticles designed to deliver drugs, and phytochemicals with multi-targeted activity. The focus of this paper is on the scientific data supporting both the mechanistic pathways underlying the damage and the pharmacological/biological therapies that might treat the damage from a single point of view. The innovative aspect of this article lies in its demonstration of the relationship between oxidative stress and inflammation and its impact on the continuum of neuronal disease causing TBI leading to AD, and the potential of multi-targeted therapies to modify the ongoing disease processes.