2021
DOI: 10.3390/life11030229
|View full text |Cite
|
Sign up to set email alerts
|

Abstract: In 1960, Rita Levi-Montalcini and Barbara Booker made an observation that transformed neuroscience: as neurons mature, they become apoptosis resistant. The following year Leonard Hayflick and Paul Moorhead described a stable replicative arrest of cells in vitro, termed “senescence”. For nearly 60 years, the cell biology fields of neuroscience and senescence ran in parallel, each separately defining phenotypes and uncovering molecular mediators to explain the 1960s observations of their founding mothers and fat… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1
1
1

Citation Types

0
22
0

Year Published

2021
2021
2024
2024

Publication Types

Select...
8
1

Relationship

0
9

Authors

Journals

citations
Cited by 29 publications
(22 citation statements)
references
References 186 publications
0
22
0
Order By: Relevance
“…In the brain, resident cellular components contain sev eral so called death receptors, such as TNFR1, FAS, and DR4, which, when interacting with TNF α and FAS L, activate the extrinsic recep tor pathway of apoptosis [12]. The receptor mech anism of apoptosis in epilepsy was previously confirmed indirectly by administering TNF α neutralizing antibodies having an in vitro neuro protective effect [13].…”
Section: Introductionmentioning
confidence: 99%
“…In the brain, resident cellular components contain sev eral so called death receptors, such as TNFR1, FAS, and DR4, which, when interacting with TNF α and FAS L, activate the extrinsic recep tor pathway of apoptosis [12]. The receptor mech anism of apoptosis in epilepsy was previously confirmed indirectly by administering TNF α neutralizing antibodies having an in vitro neuro protective effect [13].…”
Section: Introductionmentioning
confidence: 99%
“…Cell senescence is related both to aging and to neurodegenerative diseases, such as Alzheimer’s disease (AD), PD, and frontotemporal dementia. Cell cycle arrest and cell senescence are known to be some of the main causes for PD, which can activate cyclin-dependent kinase (cdk5), induce neuronal inflammasomes, and lead neuronal cells to enter a senescence-like state or death in PD [ 35 , 36 , 37 , 38 ]. In addition, cell senescence affects ECM composition and content [ 39 ].…”
Section: Discussionmentioning
confidence: 99%
“…Postnatally, the result of these orchestrated changes could be traces of the presence of abnormal neural cells during prenatal development. Alternatively, a variety of phenomena (DNA replication stress, cellular senescence [26,27]) are able to favor the conservation of CIN rates or even promote CIN progression after birth throughout adulthood. When transformed into an appreciable population, cells affected by CIN/somatic mosaicism are able to become a source for morbidity and aging [28][29][30].…”
Section: Cin In the Human Brain: An Ontogenetic Viewmentioning
confidence: 99%