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Related Concept Videos

Alzheimer's Disease: Treatment01:22

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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...
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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 (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 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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Related Experiment Video

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Automated, Long-term Behavioral Assay for Cognitive Functions in Multiple Genetic Models of Alzheimer's Disease, Using IntelliCage
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Investigating interventions in Alzheimer's disease with computer simulation models.

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Systems modelling advances Alzheimer's disease research by simulating immunotherapy. The model predicts plaque clearance but limited impact on cognitive decline markers, suggesting early or combination therapies are crucial.

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Area of Science:

  • Biomedical Research
  • Computational Biology
  • Neuroscience

Background:

  • Alzheimer's disease (AD) therapies face challenges with efficacy and side effects.
  • Systems modelling offers a valuable approach for studying age-related diseases.
  • Previous work established a model for amyloid-beta (Aβ) and tau aggregation pathways.

Purpose of the Study:

  • To extend a stochastic computer model of Alzheimer's disease.
  • To incorporate passive and active immunisation processes against Aβ.
  • To evaluate the model's predictions against neuropathological observations.

Main Methods:

  • Developed a stochastic computer model for Alzheimer's disease.
  • Integrated mechanisms of Aβ immunisation (passive and active).
  • Simulated the effects of immunisation on soluble Aβ, plaques, phosphorylated tau, and tangles.

Main Results:

  • Model predicts immunisation clears Aβ plaques.
  • Model shows minimal reduction in soluble Aβ, phosphorylated tau, and tangles.
  • Model predictions align with neuropathological findings in immunised Alzheimer's patients.

Conclusions:

  • Aβ immunotherapy may be more effective when initiated early in Alzheimer's disease.
  • Combination therapies might be necessary for significant clinical benefit.
  • Systems modelling provides insights into AD progression and therapeutic interventions.