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Related Concept Videos

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...
Alzheimer Disease l: Introduction01:29

Alzheimer Disease l: Introduction

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...
Alzheimer's Disease: Overview01:26

Alzheimer's Disease: Overview

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 and tau...
Alzheimer's Disease: Treatment01:22

Alzheimer's Disease: Treatment

Alzheimer's Disease (AD), a neurodegenerative disorder, is pathologically identified by amyloid plaques and neurofibrillary tangles composed of tau protein. AD pharmacotherapy aims to manage cognitive symptoms, delay disease progression, and treat behavioral symptoms. The treatment is primarily symptomatic and palliative, with no definitive disease-modifying therapy available. Cholinesterase inhibitors, including donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne), are...
Dementia l: Introduction01:22

Dementia l: Introduction

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...
Parkinson Disease ll: Pathophysiology01:24

Parkinson Disease ll: Pathophysiology

Parkinson disease (PD) is a progressive neurodegenerative disorder primarily affecting movement, with additional non-motor features. Its pathophysiology involves complex interactions among genetic susceptibility, environmental exposures, and cellular dysfunction, including dopaminergic neuron loss, protein aggregation, and mitochondrial impairment.Selective NeurodegenerationA key feature is the degeneration of dopaminergic neurons in the substantia nigra pars compacta, leading to reduced...

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Related Experiment Video

Updated: May 31, 2026

Visualizing Axonal Growth Cone Collapse and Early Amyloid β Effects in Cultured Mouse Neurons
06:23

Visualizing Axonal Growth Cone Collapse and Early Amyloid β Effects in Cultured Mouse Neurons

Published on: October 30, 2018

c-Abl in neurodegenerative disease.

Sarah D Schlatterer1, Christopher M Acker, Peter Davies

  • 1Department of Pathology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.

Journal of Molecular Neuroscience : MN
|July 6, 2011
PubMed
Summary

The c-Abl tyrosine kinase is implicated in neurodegenerative diseases like Alzheimer's and Parkinson's. Its activation, triggered by amyloid beta and oxidative stress, may contribute to neuronal dysfunction and pathology.

Area of Science:

  • Neurobiology
  • Cellular Biology
  • Biochemistry

Background:

  • The c-Abl tyrosine kinase regulates critical cellular processes like the cell cycle and apoptosis.
  • The Abl family of kinases is essential for central nervous system development.
  • Emerging evidence links c-Abl activation to Alzheimer's and Parkinson's disease pathology.

Purpose of the Study:

  • To explore the potential role of c-Abl in the pathogenesis of neurodegenerative diseases.
  • To contextualize c-Abl activation within known neurodegenerative mechanisms.

Main Methods:

  • Review of recent studies on c-Abl in human neurodegenerative diseases.
  • Analysis of findings from mouse models and neuronal cultures exposed to amyloid beta and oxidative stress.
  • Examination of the effects of c-Abl overexpression in adult mouse neurons.

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Main Results:

  • c-Abl activation is observed in human Alzheimer's and Parkinson's disease.
  • Amyloid beta fibrils and oxidative stress activate c-Abl in neuronal models.
  • Overexpression of active c-Abl induces neurodegeneration and neuroinflammation in mice.

Conclusions:

  • c-Abl activation is a potential contributor to the pathogenesis of neurodegenerative diseases.
  • Understanding c-Abl's role provides insight into disease mechanisms and potential therapeutic targets.