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Replicative Cell Senescence

Replicative Cell Senescence

Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds the telomeric...

Replicative Cell Senescence

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Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds the telomeric...

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Single-cell Profiling of Developing and Mature Retinal Neurons

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Single-Nucleus Profiling Reveals a BBB Senescence Unit Driving AD Pathology in Human Brain.

Yuanwei Zhang^1,2, Zhongman Jin^3,4, Ruizhen Rao^5,6

¹College of Life Sciences, University of Chinese Academy of Sciences, Beijing, 100049, China.

Molecular Neurobiology

|June 1, 2026

Summary

Cellular senescence drives Alzheimer's disease (AD) by forming a brain barrier (BBB) senescence unit. This unit involves inflammatory signaling and a SPP1-CD44 axis, highlighting senescence as a key AD pathological process.

Keywords:

Alzheimer’s disease Blood-brain barrier Cellular senescence Neurovascular unit SPP1-CD44 signaling pathway Single-nucleus transcriptomics

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Published on: June 28, 2019

Area of Science:

Neuroscience
Cell Biology
Pathology

Background:

Cellular senescence is implicated in Alzheimer's disease (AD) pathogenesis.
Its role within the neurovascular unit, particularly the blood-brain barrier (BBB), is not fully understood.

Purpose of the Study:

To elucidate the molecular mechanisms of cellular senescence in the AD neurovascular unit.
To identify key cellular players and signaling pathways involved in BBB senescence in AD.

Main Methods:

Integrated single-nucleus RNA sequencing from 75 human brain samples.
Analyzed intercellular communication and gene network interactions.
Validated findings using cerebrospinal fluid proteomics data.

Main Results:

Identified a coordinated BBB senescence unit comprising astrocytes, pericytes, microglia, and T cells.
Revealed inflammatory signaling and maladaptive repair in senescent cells.
Uncovered the SPP1-CD44 axis as central to BBB senescence, with SPP1 acting as a hub gene correlated with AD pathology scores.

Conclusions:

Cellular senescence is a critical pathological process in AD, specifically impacting the neurovascular unit.
The BBB senescence unit, driven by the SPP1-CD44 axis, contributes to AD pathogenesis through sustained inflammation.
SPP1 represents a potential therapeutic target and biomarker for AD.