Related Experiment Video

Updated: May 17, 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

Peripheral mononuclear cell rejuvenation for senescence surveillance in Alzheimer disease

Marco Malavolta1, Andrea Basso, Francesco Piacenza

  • 1Translational Research Ctr. of Nutrition and Ageing, IRCCS-INRCA, via Birarelli 8, Ancona, Italy. m.malavolta@inrca.it

Current Pharmaceutical Design
|October 16, 2012
PubMed

Insights

Senescent cells in the brain contribute to Alzheimer's disease (AD). Peripheral immune cells may help clear these cells, offering a potential therapeutic target for neurodegeneration.

Area of Science:

  • Neuroscience
  • Immunology
  • Cellular Biology

Background:

  • Cellular senescence in microglia, astrocytes, and endothelial cells is linked to Alzheimer's disease (AD) onset and progression.
  • Accumulation of senescent cells in the central nervous system (CNS) may drive neurodegeneration and age-related cognitive decline.
  • Efficient clearance of senescent cells is crucial for preventing or delaying neurodegeneration.

Purpose of the Study:

  • Investigate the clearance mechanisms of senescent cells within the CNS.
  • Hypothesize the role of peripheral mononuclear phagocytes (MP) in senescent cell surveillance in AD.
  • Explore therapeutic interventions targeting peripheral MP function for AD treatment.

Main Methods:

  • Literature review and synthesis of current research on cellular senescence in AD.
  • Analysis of the potential involvement of microglia and peripheral MP in senescent cell removal.
  • Hypothetical modeling of immune cell interactions in the AD brain.

Main Results:

  • Resident microglia are implicated in clearing senescent cells in the CNS.
  • Peripheral MP may assist microglia in managing brain inflammation and amyloid-beta (Abeta) deposits in AD.
  • Age-related dysfunction of innate immunity cells can exacerbate AD progression alongside cellular senescence.

Conclusions:

  • Peripheral MP may play a vital role in CNS senescence surveillance, especially when microglia function is impaired.
  • Targeting and rejuvenating peripheral MP function presents a promising therapeutic strategy for AD.
  • Further research is needed to elucidate the precise mechanisms of senescence clearance in the brain and develop effective interventions.

More Related Videos

Stereological Estimation of Cholinergic Fiber Length in the Nucleus Basalis of Meynert of the Mouse Brain09:15

Stereological Estimation of Cholinergic Fiber Length in the Nucleus Basalis of Meynert of the Mouse Brain

Published on: February 5, 2020

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...
Alzheimer's Disease: Treatment01:22

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...
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'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...