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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 (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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A High Throughput, Multiplexed and Targeted Proteomic CSF Assay to Quantify Neurodegenerative Biomarkers and Apolipoprotein E Isoforms Status
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CSF biomarkers: pinpointing Alzheimer pathogenesis.

Niklas Mattsson1, Kaj Blennow, Henrik Zetterberg

  • 1Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, the Sahlgrenska Academy at University of Gothenburg, S-431 80 Mölndal, Sweden.

Annals of the New York Academy of Sciences
|November 13, 2009
PubMed
Summary

This review explores cerebrospinal fluid (CSF) biomarkers for inflammation, oxidative stress, and mitochondrial dysfunction in Alzheimer's disease (AD) pathogenesis. It assesses their clinical and trial utility beyond amyloid and tau.

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Area of Science:

  • Neuroscience
  • Biochemistry
  • Pathology

Background:

  • Alzheimer's disease (AD) pathogenesis research has historically focused on amyloid and tau pathologies.
  • Increasing evidence highlights the significant roles of inflammation, oxidative stress, and mitochondrial dysfunction in AD.
  • These factors contribute to synaptic and neuronal loss, exacerbating disease progression.

Purpose of the Study:

  • To review available cerebrospinal fluid (CSF) biomarkers associated with inflammation, oxidative stress, and mitochondrial dysfunction in Alzheimer's disease.
  • To evaluate the potential clinical utility of these biomarkers.
  • To assess their applicability in clinical trials for AD.

Main Methods:

  • Comprehensive literature review of studies reporting CSF biomarkers for inflammation, oxidative stress, and mitochondrial dysfunction.
  • Analysis of biomarker data in the context of Alzheimer's disease pathogenesis.
  • Evaluation of current clinical and research applications of identified biomarkers.

Main Results:

  • Several CSF biomarkers reflecting inflammation (e.g., IL-6, TNF-α), oxidative stress (e.g., F2-isoprostanes), and mitochondrial dysfunction (e.g., mtDNA) are available.
  • These biomarkers show potential for tracking disease progression and therapeutic response.
  • Their standardization and validation are crucial for widespread clinical adoption.

Conclusions:

  • CSF biomarkers beyond amyloid and tau are essential for a comprehensive understanding of Alzheimer's disease.
  • These biomarkers offer promising avenues for early diagnosis, monitoring disease activity, and evaluating treatment efficacy in clinical trials.
  • Further research is needed to standardize assays and validate their use in diverse patient populations.