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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 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...
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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...
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Hepatic Encephalopathy

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Related Experiment Videos

Elevated 4-hydroxyhexenal in Alzheimer's disease (AD) progression.

Melissa A Bradley1, Shuling Xiong-Fister, William R Markesbery

  • 1Department of Chemistry, University of Kentucky, Lexington, KY 40536, USA.

Neurobiology of Aging
|October 23, 2010
PubMed
Summary

Elevated levels of 4-hydroxyhexenal (HHE), a lipid peroxidation product, were found in Alzheimer

Related Experiment Videos

Area of Science:

  • Neuroscience
  • Biochemistry
  • Pathology

Background:

  • Elevated α, β-unsaturated aldehydes like HNE and acrolein are implicated in Alzheimer's disease (AD) progression.
  • 4-hydroxyhexenal (HHE), a lipid peroxidation product of ω-3 PUFAs, has been understudied in AD.
  • Understanding HHE's role is crucial for elucidating AD pathogenesis.

Purpose of the Study:

  • To quantify extractable and protein-bound HHE levels in specific brain regions across AD stages.
  • To investigate the impact of HHE on neuronal survival and glucose uptake.
  • To determine HHE's contribution to Alzheimer's disease progression.

Main Methods:

  • Quantification of HHE (extractable and protein-bound) in hippocampus, temporal gyri, and cerebellum from normal controls and AD subjects (MCI, PCAD, LAD).
  • Assessment of HHE's effects on primary cortical neuron survival and glucose uptake in vitro.
  • Analysis of HHE levels in relation to disease severity and brain region.

Main Results:

  • Both extractable and protein-bound HHE levels were elevated in multiple brain regions during AD progression.
  • Significant increases in extractable HHE were observed in the hippocampus of PCAD and LAD subjects.
  • Protein-bound HHE was significantly higher in the hippocampus across MCI, PCAD, and LAD stages.
  • HHE exposure led to decreased neuronal survival and glucose uptake in a time- and concentration-dependent manner.

Conclusions:

  • Lipid peroxidation, specifically involving HHE, plays a significant role in Alzheimer's disease pathogenesis.
  • HHE accumulation in the brain correlates with AD progression and neurodegenerative processes.
  • These findings highlight HHE as a potential biomarker and therapeutic target in AD.