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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'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...
Dementia01:30

Dementia

Dementia is a collective term for cognitive disorders primarily affecting memory, thinking, and reasoning. It is not a specific disease but a syndrome, with Alzheimer's disease being the most common cause, accounting for approximately 60-80% of cases. Other types include vascular dementia, Lewy body dementia, and frontotemporal dementia. Dementia affects millions worldwide, particularly older adults, though it is not a normal part of aging.
The progression of dementia is generally gradual.
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 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...
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: Jul 11, 2026

Author Spotlight: Stimulation-Based Approach to Improve Cerebral Blood Flow in Alzheimer's Model
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Special Issue: Alzheimer's disease.

Khue Vu Nguyen1,2

  • 1Department of Medicine, Biochemical Genetics and Metabolism, The Mitochondrial and Metabolic Disease Center, School of Medicine, University of California, San Diego, Building CTF, Room C-103, 214 Dickinson Street, San Diego, CA 92103-8467, USA.

AIMS Neuroscience
|April 29, 2020
PubMed
Summary

Alzheimer's disease (AD) impacts millions globally, driven by aging. New research suggests alternative therapeutic strategies beyond the amyloid hypothesis, focusing on gene expression and interactions.

Keywords:
Alzheimer's diseaseAmyloid-β (Aβ) peptidesEpigenetic modificationsFamilial AD (FAD)Neurofibrillary tangles (NFTs)Sporadic AD (SAD)gene-gene and/or gene-environment interactionsβ-amyloid precursor protein (APP)

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Area of Science:

  • Neuroscience
  • Genetics
  • Epidemiology

Background:

  • Alzheimer's disease (AD) affects over 45 million worldwide, with age as the primary risk factor, projected to reach 131 million by 2050.
  • The amyloid hypothesis, proposing amyloid-β (Aβ) peptide deposition drives neurodegeneration, has been the focus for over two decades.
  • Current AD treatments offer symptomatic relief but do not halt disease progression.

Discussion:

  • Emerging evidence indicates neuronal-injury biomarkers are independent of Aβ, suggesting epigenetic modifications and gene interactions in AD etiology.
  • This necessitates a re-evaluation of the pathological cascade and exploration of alternative therapeutic strategies.
  • Research into the expression of β-amyloid precursor protein (APP) gene and its various mRNA isoforms is crucial for understanding disease risk.

Key Insights:

  • Neuronal-injury biomarkers suggest AD pathogenesis may involve factors beyond Aβ accumulation.
  • Alternative therapeutic strategies and a deeper understanding of APP gene expression are needed.
  • Investigating gene-gene and gene-environment interactions offers new avenues for AD research.

Outlook:

  • Further research into the physiological function of the β-amyloid precursor protein (APP) is essential for a comprehensive understanding of AD.
  • Identifying key APP-mRNA isoforms could provide insights into normal function versus disease risk.
  • Developing novel biomarkers and therapeutic targets independent of the amyloid hypothesis is a critical future direction.