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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...
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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.
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Alzheimer Disease l: Introduction

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Amyloid Fibrils03:03

Amyloid Fibrils

Amyloid fibrils are aggregates of misfolded proteins.  Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils. 
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Amyloid Fibrils03:03

Amyloid Fibrils

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Updated: May 27, 2026

Biochemical Purification and Proteomic Characterization of Amyloid Fibril Cores from the Brain
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Published on: April 28, 2022

Biochemical alterations associated with ALS.

Kay A Lawton1, Merit E Cudkowicz, Meredith V Brown

  • 1Metabolon Inc., North Carolina, USA.

Amyotrophic Lateral Sclerosis : Official Publication of the World Federation of Neurology Research Group on Motor Neuron Diseases
|November 26, 2011
PubMed
Summary
This summary is machine-generated.

This study used metabolomics to find altered metabolic pathways in amyotrophic lateral sclerosis (ALS) patients. Key biochemical changes suggest new therapeutic targets and diagnostic biomarkers for ALS.

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Area of Science:

  • Biochemistry
  • Neuroscience
  • Metabolomics

Background:

  • Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease with complex pathophysiology.
  • Identifying key metabolic alterations in ALS is crucial for developing effective treatments and diagnostic tools.

Purpose of the Study:

  • To identify metabolic pathways affected in ALS patients using non-targeted metabolomics.
  • To discover potential therapeutic targets and diagnostic biomarkers for ALS based on metabolic signatures.

Main Methods:

  • Cross-sectional studies involving plasma samples from ALS patients and healthy controls.
  • Global metabolic profiling to detect and evaluate biochemical signatures associated with ALS.
  • Statistical analysis to identify significantly altered metabolites in ALS patient plasma.

Main Results:

  • Twenty-three metabolites were significantly altered in plasma from ALS patients across both studies.
  • Altered metabolites are involved in pathways related to neuronal damage, hypermetabolism, oxidative stress, and mitochondrial dysfunction.
  • Evidence suggests potential hepatic dysfunction associated with ALS.

Conclusions:

  • Metabolomics analysis provides insights into ALS pathophysiology.
  • Identified metabolic alterations highlight potential therapeutic targets and diagnostic biomarkers for ALS.
  • This approach can generate novel hypotheses for future ALS research.