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Related Concept Videos

Alzheimer Disease ll: Pathophysiology01:23

Alzheimer Disease ll: Pathophysiology

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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...
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Huntington Disease l: Introduction01:21

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Huntington disease or HD is a progressive, fatal neurodegenerative disorder inherited in an autosomal dominant pattern.PathophysiologyIt is caused by expansion of the CAG trinucleotide repeat in the HTT gene on chromosome 4 (4p16.3), producing an abnormal huntingtin protein with an expanded polyglutamine tract. This misfolded protein disrupts cellular function, leading to neuronal death. Normal alleles have ≤26 repeats, 27–35 are intermediate (risk of expansion), 36–39 show...
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Aging is a complex biological phenomenon influenced by various processes that affect cellular and systemic functions. Several prominent theories attempt to explain its mechanisms, highlighting cellular limitations, oxidative damage, and hormonal changes as central factors in aging.
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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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Alzheimer's Disease: Overview01:26

Alzheimer's Disease: Overview

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Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
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Alzheimer disease is a chronic, progressive, and irreversible neurodegenerative disorder and the most common cause of dementia in older adults. It leads to gradual neuronal loss, causing cognitive decline, behavioral changes, and loss of functional independence.Risk Factors and EtiologyThe disease is multifactorial. Age is the strongest risk factor, with prevalence doubling every 5 years after age 65. Genetic factors include mutations in genes such as APP, PSEN1, and PSEN2, which are associated...
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Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology
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ShcC proteins: brain aging and beyond.

Orli Sagi1, Arie Budovsky2, Marina Wolfson1

  • 1The Shraga Segal Department of Microbiology, Immunology and Genetics, Center for Multidisciplinary Research on Aging, Ben-Gurion University of the Negev, Beer Sheva 84105, Israel.

Ageing Research Reviews
|December 3, 2014
PubMed
Summary
This summary is machine-generated.

The ShcC protein, less studied than ShcA, is crucial for neuroprotection against aging brain conditions like ischemia and oxidative stress. This review covers ShcC

Keywords:
AgingBrain ischemiaBrain tumorsImmunityShcC adaptor proteinsSignaling

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Area of Science:

  • Neuroscience and Molecular Biology
  • Cellular Signaling and Aging Research

Background:

  • The Shc family of signaling adaptor proteins plays a role in cellular communication.
  • Most research has focused on the ShcA protein, with less attention paid to the neuronal ShcC protein.
  • Emerging evidence highlights ShcC's potential role in neuroprotection against age-related conditions.

Purpose of the Study:

  • To review over a decade of research on the expression and function of the ShcC protein.
  • To explore ShcC's role in normal brain function, age-related brain pathologies, and immune disorders.
  • To focus on ShcC's interactions with signaling proteins and pathways relevant to aging.

Main Methods:

  • Literature review of studies on ShcC expression and function.
  • Analysis of ShcC's involvement in neuroprotection against brain ischemia and oxidative stress.
  • Examination of ShcC's interactions with signaling molecules in the context of aging.

Main Results:

  • ShcC is important for neuroprotection in aging-associated conditions.
  • ShcC expression and function are relevant in normal brain, brain pathologies, and immune disorders.
  • ShcC interacts with key signaling proteins and pathways implicated in aging processes.

Conclusions:

  • The neuronal ShcC protein is a significant factor in neuroprotection against age-related brain insults.
  • Understanding ShcC's signaling interactions is key to deciphering its role in aging.
  • Further research into ShcC may offer insights into therapeutic strategies for age-related neurological decline.