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Related Concept Videos

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 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: 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...

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Related Experiment Video

Updated: Jun 5, 2026

Transcranial Pulse Stimulation for Alzheimer's Patients
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Transcranial Pulse Stimulation for Alzheimer's Patients

Published on: April 4, 2025

APP processing in Alzheimer's disease.

Yun-wu Zhang1, Robert Thompson, Han Zhang

  • 1Institute for Biomedical Research, Xiamen University, 422 SiMingNanLu, Xiamen 361005, Fujian, PR China.

Molecular Brain
|January 11, 2011
PubMed
Summary
This summary is machine-generated.

Alzheimer

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Examining the Characteristics of Episodic Memory using Event-related Potentials in Patients with Alzheimer's Disease
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Published on: August 30, 2011

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Examining the Characteristics of Episodic Memory using Event-related Potentials in Patients with Alzheimer's Disease
11:01

Examining the Characteristics of Episodic Memory using Event-related Potentials in Patients with Alzheimer's Disease

Published on: August 30, 2011

Area of Science:

  • Neuroscience and Neurodegenerative Diseases
  • Molecular Biology and Biochemistry

Background:

  • Alzheimer's disease (AD) is characterized by brain senile plaques, primarily composed of amyloid-beta (Aβ) peptides.
  • Aβ overproduction and aggregation are considered key drivers of AD pathogenesis.
  • Targeting Aβ generation pathways is a significant focus in AD therapeutic research.

Purpose of the Study:

  • To review current understanding of amyloid precursor protein (APP) processing.
  • To explore the regulation of APP metabolism and its physiological roles.
  • To discuss the pathological functions of APP and its metabolites in AD.

Main Methods:

  • Literature review of existing research on APP processing and its relation to AD.
  • Analysis of enzymatic pathways involved in APP cleavage (β-secretase, γ-secretase, α-secretase, caspases).
  • Synthesis of information on the physiological and pathological significance of APP and its derivatives.

Main Results:

  • APP can be processed via amyloidogenic (β- and γ-secretase) or non-amyloidogenic (α-secretase) pathways.
  • Alternative cleavage by caspases may also contribute to AD pathology.
  • Understanding these diverse processing routes is vital for therapeutic strategies.

Conclusions:

  • Modulating APP processing represents a promising therapeutic avenue for Alzheimer's disease.
  • Further research into APP metabolism and the functions of its fragments is essential for developing effective treatments.
  • Targeting secretase activity offers potential for inhibiting Aβ generation and mitigating AD progression.