在前段缺血光学神经病变患者中,功能性脑网络的异常拓组织

Fei Chen1, Xin-Miao Wang2, Xin Huang3

  • 1Department of Opthalmology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.

Frontiers in neuroscience
|December 9, 2024
PubMed
概括

前段缺血视神经病变 (AION) 患者表现出大脑连接的改变,局部效率降低和网络变化. 这些发现揭示了AION视觉损失和认知问题的神经基础.

相关概念视频

Neural Regulation01:37

Neural Regulation

Digestion begins with a cephalic phase that prepares the digestive system to receive food. When our brain processes visual or olfactory information about food, it triggers impulses in the cranial nerves innervating the salivary glands and stomach to prepare for food.
Brain Imaging01:14

Brain Imaging

Brain imaging technologies provide critical insights into both the structure and function of the human brain, enabling medical professionals and researchers to diagnose, study, and treat neurological disorders or psychiatric disorders more effectively.
These technologies include computerized axial tomography (CAT or CT scans), positron-emission tomography (PET scans),  magnetic resonance imaging (MRI),  functional magnetic resonance imaging (fMRI), and Transcranial Magnetic Stimulation (TMS).
Prosopagnosia01:24

Prosopagnosia

Prosopagnosia, also known as face blindness, is the inability to recognize faces. In severe cases, individuals with prosopagnosia may not recognize close family members, including parents and spouses, by their faces. For instance, someone with prosopagnosia might walk past their child in a crowd, only realizing their mistake upon noticing their child's distinctive backpack or favorite jacket. Prosopagnosia specifically impairs facial recognition, while the recognition of other objects or...
Alzheimer Disease ll: Pathophysiology01:23

Alzheimer Disease ll: Pathophysiology

Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and microglia. Abnormal...