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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...
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Dementia is an acquired, progressive syndrome characterized by a decline in multiple cognitive domains severe enough to impair daily functioning and reduce independence. Although memory loss is a central feature, the diagnosis requires additional deficits involving language, executive function, visuospatial skills, judgment, calculation, or abstract reasoning. These cognitive impairments reflect underlying neurodegenerative or vascular processes that gradually disrupt neuronal networks...
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Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...
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Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this barrier loses...
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[Brain atrophy in clinically isolated syndrome].

J I Rojas1, L Patrucco, C Besada

  • 1Servicio de Neurología, Hospital Italiano, Buenos Aires, Argentina. juan.rojas@hospitalitaliano.org.ar

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Brain atrophy, particularly gray matter loss, is evident in clinically isolated syndrome (CIS) patients, indicating early disease progression in multiple sclerosis (MS). This finding highlights the need for early intervention in MS.

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Area of Science:

  • Neurology
  • Radiology

Context:

  • Multiple Sclerosis (MS) is characterized by early brain atrophy.
  • Clinically Isolated Syndrome (CIS) represents an early stage of MS.

Purpose:

  • To investigate the presence and extent of brain atrophy in patients with CIS compared to healthy controls.
  • To assess total brain volume (TBV), gray matter volume (GMV), and white matter volume (WMV) in CIS patients.

Summary:

  • A prospective study compared 20 CIS patients with 30 age- and gender-matched healthy controls.
  • Automated analysis using SIENAX revealed significantly reduced TBV, GMV, and WMV in CIS patients.
  • GMV showed the most pronounced reduction, indicating significant gray matter atrophy in early MS stages.

Impact:

  • This study provides the first evidence of brain atrophy in a Latin American CIS cohort.
  • Findings suggest that neurodegeneration, especially gray matter loss, occurs early in the MS disease course.
  • Early detection of brain atrophy in CIS may inform future therapeutic strategies and prognosis.