Cited by 95Cancer-related Molecular PathwaysGenetics, Aging, and Longevity in Model OrganismsTelomeres, Telomerase, and Senescence

p53 at the crossroads between cancer and neurodegeneration

Lanni, Cristina, Racchi, Marco, Memo, Maurizio, Govoni, Stefano, Uberti, Daniela·2012·Free Radical Biology and Medicine

Abstract

Aging, dementia, and cancer share a critical set of altered cellular functions in response to DNA damage, genotoxic stress, and other insults. Recent data suggest that the molecular machinery involved in maintaining neural function in neurodegenerative disease may be shared with oncogenic pathways. Cancer and neurodegenerative diseases may be influenced by common signaling pathways regulating the balance of cell survival versus death, a decision often governed by checkpoint proteins. This paper focuses on one such protein, p53, which represents one of the most extensively studied proteins because of its role in cancer prevention and which, furthermore, has been recently shown to be involved in aging and Alzheimer disease (AD). The contribution of a conformational change in p53 to aging and neurodegenerative processes has yet to be elucidated. In this review we discuss the multiple functions of p53 and how these correlate between cancer and neurodegeneration, focusing on various factors that may have a role in regulating p53 activity. The observation that aging and AD interfere with proteins controlling duplication and cell cycle may lead to the speculation that, in senescent neurons, aberrations in proteins generally dealing with cell cycle control and apoptosis could affect neuronal plasticity and functioning rather than cell duplication.

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Registry

Crossref · 10.1016/j.freeradbiomed.2012.02.034

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124 of 124 references verified0 citation errors · 0 not checkable

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  • Increased or altered p53 activity is found to correlate with AD.

    “Increased or altered p53 activity is found to correlate with AD (Lanni et al., 2012), and animal model studies implicate a PARP-dependent programmed-necrosis pathway in PD (Lee et al., 2014).”

    From Programmed cell death in aging (2015) · cites this paper as Lanni et al., 2012

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Authors
Lanni, C., Racchi, M., Memo, M., Govoni, S., & Uberti, D.
Affiliations
  • University of Pavia (IT)
  • University of Brescia (IT)
Corresponding author
Lanni, Cristina
Venue
Free Radical Biology and Medicine
Publisher
Elsevier BV
Published
2012-05
Volume
52
Issue
9
Pages
1727-1733
ISSN
0891-5849 (ISSN-L)
OpenAlex
W1981859966
Cited by
95
References
124
Citations by year
2026: 4 · 2025: 3 · 2024: 5 · 2023: 5 · 2022: 1 · 2021: 5 · 2020: 10 · 2019: 6 · 2018: 4 · 2017: 8 · 2016: 4 · 2015: 14 · 2014: 8 · 2013: 15 · 2012: 3
FWCI
1.32
Type
journal article
Language
en
Open access
closed
Locations
  • Free Radical Biology and Medicine (publishedVersion)
  • PubMed (publishedVersion)
  • Institutional Research Information System (Università degli Studi di Brescia) (submittedVersion)
Funders
  • Centre International de Recherche sur le Cancer
  • Regione Lombardia
Topics
  • Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
  • Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
Keywords
p53, neurodegeneration, Alzheimer's disease, aging, cancer, DNA damage response, genotoxic stress, neuronal senescence, apoptosis, cell cycle regulation, neuroplasticity, checkpoint proteins
MeSH terms
Humans, Mutation, Neoplasms, Genes, p53, Neurodegenerative Diseases

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