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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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Alzheimer Disease l: Introduction01:29

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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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Alzheimer's Disease: Overview01:26

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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.
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ...
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Dementia l: Introduction01:22

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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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Cellular Injury IV: Necrosis01:16

Cellular Injury IV: Necrosis

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Necrosis is a form of irreversible cell death caused by severe injury such as ischemia, toxins, or trauma. Unlike programmed cell death, it is an uncontrolled, pathological process that typically provokes inflammation in surrounding tissues.Pathophysiologic ChangesNecrosis begins when cells sustain critical damage, leading to swelling of organelles, particularly mitochondria, and rapid ATP depletion. As energy levels decline, membrane ion pumps fail, leading to calcium influx and eventually,...
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Amyloid Fibrils03:03

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Amyloid fibrils are aggregates of misfolded proteins.  Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils. 
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Subcellular injuries in Alzheimer's disease.

Jean-Paul Tillement, Vassilios Papadopoulos1

  • 1Research Institute of the McGill University Health Center, Montreal General Hospital, 1650 Cedar Avenue, C10-148, Montreal, Quebec H3G 1A4, Canada. vassilios.papadopoulos@mcgill.ca.

CNS & Neurological Disorders Drug Targets
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Alzheimer's disease begins with subcellular injuries at the Golgi apparatus, preceding amyloid buildup. This sequence leads to neuroinflammation and cell death, offering potential new drug targets.

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Pathology

Background:

  • Alzheimer's disease (AD) is a leading cause of dementia in older adults.
  • Multiple hypotheses exist for AD pathophysiology, including amyloidogenesis and tau hyperphosphorylation.
  • Understanding the sequence of subcellular events is crucial for identifying therapeutic targets.

Purpose of the Study:

  • To review and sequence subcellular injuries in Alzheimer's disease (AD).
  • To correlate cellular and subcellular events with neurodegeneration and cell death in AD.
  • To identify the earliest subcellular defects initiating AD pathogenesis.

Main Methods:

  • Review of experimental models, clinical symptoms, and autopsy reports of AD.
  • Analysis of the temporal order of subcellular events in AD pathogenesis.
  • Examination of the role of Golgi apparatus, lysosomes, and inflammatory processes.

Main Results:

  • Subcellular injuries initiate at the Golgi apparatus before beta-amyloid deposition.
  • Lysosomal dysfunction and impaired beta-amyloid clearance follow Golgi alterations.
  • Neuroinflammation, originating in intracellular organelles, precedes widespread neurodegeneration and cell death.

Conclusions:

  • The sequence of subcellular events in AD begins with Golgi apparatus injury.
  • Lysosomal dysfunction and intracellular inflammation are key steps leading to neurodegeneration.
  • Identifying the precise sequence of events may reveal novel therapeutic targets for Alzheimer's disease.