Related Experiment Video

Updated: Jul 16, 2026

Measurement of Protein Turnover Rates in Senescent and Non-Dividing Cultured Cells with Metabolic Labeling and Mass Spectrometry
08:52

Measurement of Protein Turnover Rates in Senescent and Non-Dividing Cultured Cells with Metabolic Labeling and Mass Spectrometry

Published on: April 6, 2022

Evidence that aging and amyloid promote microglial cell senescence

Barry E Flanary1, Nicole W Sammons, Cuong Nguyen

  • 1Department of Neuroscience, University of Florida College of Medicine, McKnight Brain Institute, Gainesville, Florida 32610-0244, USA.

Rejuvenation Research
|March 24, 2007
PubMed

Insights

Microglial cells experience telomere shortening with aging, a process worsened by amyloid deposits. This cellular aging and degeneration in microglia contribute to the development of Alzheimer

Area of Science:

  • Neuroscience
  • Cell Biology
  • Gerontology

Background:

  • Advanced age and amyloid deposits are key risk factors for Alzheimer's disease (AD) neurodegeneration.
  • Microglial activation is observed in AD, but its precise role in pathogenesis is unclear.

Purpose of the Study:

  • To investigate the impact of aging and amyloid on microglial cell health and function.
  • To determine if microglial senescence is linked to Alzheimer's disease development.

Main Methods:

  • Analysis of telomere length and telomerase activity in rat microglial cells during normal aging.
  • Examination of telomere shortening trends in human brain samples from individuals with and without dementia.
  • Assessment of microglial dystrophy in human brains with varying amyloid loads.

Main Results:

  • Microglial cells showed significant telomere shortening and reduced telomerase activity with normal aging in rats.
  • A trend towards telomere shortening was observed in human brains with dementia.
  • Human brains with high amyloid loads exhibited greater microglial dystrophy compared to controls.

Conclusions:

  • Microglial cell senescence, characterized by telomere shortening, is a normal aging process.
  • This senescence is exacerbated by the presence of amyloid deposits, suggesting a link to AD.
  • Microglial degeneration is proposed as a contributing factor in Alzheimer's disease pathogenesis.

More Related Videos

Primary Cultures of Rat Astrocytes and Microglia and Their Use in the Study of Amyotrophic Lateral Sclerosis09:36

Primary Cultures of Rat Astrocytes and Microglia and Their Use in the Study of Amyotrophic Lateral Sclerosis

Published on: June 23, 2022

Quantitative 3D In Silico Modeling (q3DISM) of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease09:33

Quantitative 3D In Silico Modeling (q3DISM) of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease

Published on: December 26, 2016

Related Concept Videos

Aging01:26

Aging

Aging is a complex biological phenomenon influenced by various processes that affect cellular and systemic functions. Several prominent theories attempt to explain its mechanisms, highlighting cellular limitations, oxidative damage, and hormonal changes as central factors in aging.
Cellular Clock Theory
The cellular clock theory posits that the human lifespan is closely tied to the finite capacity of cells to divide, a phenomenon governed by telomeres, which are protective caps at the ends of...
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. 
Amyloid deposits were observed as early as 1639 in the liver and the spleen.   In 1854, Rudolph Virchow performed iodine staining, normally used to...
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...
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,...
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...
The Effect of Aging on Tissues01:19

The Effect of Aging on Tissues

Several body functions deteriorate with age. The external signs of aging are easily identifiable. For example, the skin becomes dry, less elastic, and thins out, forming wrinkles. The skin of the face begins to appear looser due to a decrease in the levels of elastic and collagen fibers in the connective tissue. Additionally, melanin production in the hair follicle decreases with age, resulting in gray hair. Moreover, the senses of sight and hearing decline, so glasses and hearing aids may...