Related Experiment Video

Updated: Jul 6, 2026

LC-MS Analysis of Human Platelets as a Platform for Studying Mitochondrial Metabolism
06:04

LC-MS Analysis of Human Platelets as a Platform for Studying Mitochondrial Metabolism

Published on: April 4, 2016

Effects of ageing and Alzheimer's disease on mitochondrial function of human platelets

Chun Shi1, Kaihua Guo, David T Yew

  • 1Department of Anatomy, Zhongshan School of Medicine, Sun Yat-Sen University Guangzhou, Guangdong 510080, China.

Experimental Gerontology
|March 25, 2008
PubMed

Insights

Platelet mitochondrial function declines with age and Alzheimer's disease (AD). However, AD patient and aged platelets show resistance to amyloid-beta damage, suggesting platelets as potential biomarkers for aging and neurodegenerative diseases.

Area of Science:

  • Mitochondrial biology
  • Neurodegenerative disease research
  • Biomarker discovery

Background:

  • Mitochondrial dysfunction is implicated in aging and neurodegenerative diseases like Alzheimer's disease (AD).
  • Platelets, easily accessible blood components, contain mitochondria and can be studied for cellular health.
  • Assessing mitochondrial membrane potential and ATP levels in platelets offers insights into cellular energy metabolism and dysfunction.

Purpose of the Study:

  • To investigate mitochondrial function in platelets of Alzheimer's disease (AD) patients and aged individuals.
  • To examine the impact of beta-amyloid peptide (Abeta) on platelet mitochondrial function.
  • To determine the potential of blood platelets as biomarkers for aging and AD-related mitochondrial dysfunction.

Main Methods:

  • Measurement of platelet mitochondrial membrane potential using JC-1 fluorescence ratio.
  • Quantification of platelet adenosine 5'-triphosphate (ATP) content.
  • Establishment of an Abeta-induced platelet damage model for comparative analysis.

Main Results:

  • Younger individuals exhibited higher platelet mitochondrial membrane potential compared to AD patients and aged controls.
  • Platelet ATP levels did not significantly differ across young, aged, and AD groups.
  • Abeta exposure significantly reduced mitochondrial potential and ATP in young and aged platelets, but not in AD patient platelets, indicating resistance to Abeta-induced damage.
  • Aged platelets showed less reduction in mitochondrial potential than young platelets after Abeta exposure.

Conclusions:

  • Mitochondrial dysfunction is associated with the aging process.
  • Platelet mitochondria in AD patients and aged individuals display a tolerance to Abeta-induced damage.
  • Blood platelets may serve as valuable biomarkers for assessing mitochondrial function and age-related diseases, including Alzheimer's disease.

More Related Videos

Using Live Cell STED Imaging to Visualize Mitochondrial Inner Membrane Ultrastructure in Neuronal Cell Models08:48

Using Live Cell STED Imaging to Visualize Mitochondrial Inner Membrane Ultrastructure in Neuronal Cell Models

Published on: June 30, 2023

Related Concept Videos

Mitochondria01:37

Mitochondria

Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...
Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...
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...
Structure and Function of Platelets01:18

Structure and Function of Platelets

The cell fragments known as platelets are disc-shaped, with an average diameter of about 3 μm and a thickness of roughly 1 μm. They play a crucial role in the body's vascular clotting system, which also involves plasma proteins, blood cells, and blood vessel tissues.
Platelets are continually replenished, circulating in the bloodstream for 9-12 days before being removed by phagocytes, primarily in the spleen. A microliter of circulating blood contains between 150,000 and 450,000 platelets, with...
Mitochondrial Membranes01:45

Mitochondrial Membranes

A single mitochondrion is a bean-shaped organelle enclosed by a double-membrane system. The outer membrane of mitochondria is smooth and contains many porins - the integral membrane transporters. Porins enable free diffusion of ions and small uncharged molecules through the outer mitochondrial membrane but limit the transport of molecules larger than 5000 Daltons. Further, the outer mitochondrial membrane forms a unique structure called membrane contact sites with other subcellular organelles,...
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...