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Infection01:20

Infection

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When a pathogen enters the body and reproduces, it can cause an infection, damage body cells, and cause illness symptoms that eventually lead to disease. Therefore, its prevention requires breaking the chain of infection.
The chain begins with pathogens: bacteria, viruses, fungi, prions, or parasites such as protozoa helminths. These can be present on the skin as transient or resident flora, or they can be acquired from the environment. Identifying and treating the type of infection and...
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Urinary Tract Infection II: Pathophysiology01:25

Urinary Tract Infection II: Pathophysiology

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The pathophysiology of urinary tract infections (UTIs) encompasses several progressive stages, beginning with bacterial colonization and culminating in potential systemic complications if untreated. UTIs are primarily initiated by bacteria, such as Escherichia coli, which often originate from the gastrointestinal tract and migrate to the urinary system through the periurethral area. This migration can occur via several routes, including improper hygiene practices, sexual activity, or...
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Cystic Fibrosis: Pathogenesis01:23

Cystic Fibrosis: Pathogenesis

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Cystic fibrosis (CF), an autosomal recessive disorder, significantly affects the function of exocrine glands. This genetically inherited disease is characterized by the production of thick and sticky mucus, which can severely affect various organs and systems in the body.
CF is primarily caused by a genetic mutation in a chromosome 7 gene coding for the cystic fibrosis transmembrane conductance regulator (CFTR) protein. The most common gene mutation leading to CF is the ΔF508 mutation,...
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Pneumonia II: Pathophysiology01:29

Pneumonia II: Pathophysiology

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The pathophysiology of pneumonia involves the following steps:
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Stages of Infection01:26

Stages of Infection

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Stages of infection describe what happens to a susceptible host once a pathogen invades the human body. The stages of infection are incubation, prodromal, illness, stage of decline, and convalescence. The incubation stage is the period from exposure to a pathogen until symptoms start. The infected person is unaware of impending illness as the pathogens grow and multiply within the body. The duration may vary depending on the type of infection. The incubation period of measles averages ten to...
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Defense Against Bacterial Pathogens01:31

Defense Against Bacterial Pathogens

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The human immune system is a complex network of cells, tissues, and organs that work together to defend the body against bacterial infections. It consists of various immune cells, each playing a specific role in the defense mechanism.
Phagocytes
Phagocytes are the frontline soldiers of the immune system. They include neutrophils and macrophages. Neutrophils are the most abundant type of white blood cell and are quickly mobilized to the site of infection. Macrophages are larger cells that patrol...
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Updated: Jan 7, 2026

Mouse Footpad Inoculation Model to Study Viral-Induced Neuroinflammatory Responses
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TDP-43病変の形態学的特徴:LATEとアルツハイマー病の合併病理における比較

Sandra O Tomé1, Klara Gawor1, Christine A F von Arnim2

  • 1Laboratory of Neuropathology, KU Leuven, Leuven, Vlaams-Brabant, Belgium.

Alzheimer's & dementia : the journal of the Alzheimer's Association
|December 28, 2025
PubMed
まとめ
この要約は機械生成です。

TDP-43タンパク質病理は、辺縁優位型加齢性TDP-43脳症(LATE)とアルツハイマー病(AD)の合併病理で異なる。純粋LATEは異なるTDP-43病変パターンを示し、認知症における異なる凝集メカニズムが示唆される。

キーワード:
TDP-43LATEアルツハイマー病病理認知症

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関連する実験動画

Last Updated: Jan 7, 2026

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科学分野:

  • 神経病理学; 神経科学; 老年医学

背景:

  • 辺縁優位型加齢性TDP-43脳症(LATE)は、新たに同定された認知症の原因である。; LATEとアルツハイマー病(AD)は臨床症状を共有し、神経病理学的にしばしば併存する。; 認知症におけるTDP-43病変の形態学的特徴は、さらなる調査が必要である。

研究 の 目的:

  • 純粋LATEおよび併存するアルツハイマー病神経病理学的変化(ADNC)を有する症例におけるTDP-43病変の形態および免疫反応性種を調査すること。; LATE-NCとADNC+LATE-NCにおけるTDP-43タンパク質病変の組織病理学的特徴を鑑別すること。

主な方法:

  • 70例のヒト剖検脳組織(海馬、扁桃体、皮質)を用いた免疫組織化学検査。; TDP-43神経細胞質内封入体(NCIs)および神経突起変性(DNs)の半定量的評価。; 様々なTDP-43種(pS409/410、pS409/pS403、pS403/pS404、C末端およびN末端TDP-43)の分析。

主要な成果:

  • 純粋LATE-NC症例では、海馬における神経突起変性のバンド様パターンが主に認められた。; 純粋LATE-NC症例では、ADNC+LATE-NC症例と比較して、海馬、扁桃体、側頭皮質における神経突起変性の負担がより重度であった。; ADNC+LATE-NC症例では、扁桃体における神経細胞質内封入体の優位性が高く、TDP-43種プロファイルが異なっていた。

結論:

  • TDP-43タンパク質病変の組織病理学的特徴は、純粋LATE-NCと併存するADNCとで異なる。; LATE-NCは、中等度から高レベルのADNCの存在によって修飾されるように見える。; 異なる認知症におけるTDP-43凝集の根底にあるメカニズムは異なる可能性があり、併存する病理は互いに影響し合う。