Commitment of protein p53 and amyloid-beta peptide (Aβ) in aging of human cerebellum

Protein p53 is known to induce the cell cycle arrest and apoptosis in response to a variety of cellular distress signals and DNA damage. A recent study has demonstrated that in blood cells of aging subjects, p53 may induce early pathological changes that precede the amyloidogenic cascade. However, i...

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Published inFolia neuropathologica Vol. 2; no. 2; pp. 161 - 167
Main Authors Maślińska, Danuta, Laure-Kamionowska, Milena, Szukiewicz, Dariusz, Maśliński, Sławomir, Księżopolska-Orłowska, Krystyna
Format Journal Article
LanguageEnglish
Published Poland Termedia Publishing House 01.01.2017
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Abstract Protein p53 is known to induce the cell cycle arrest and apoptosis in response to a variety of cellular distress signals and DNA damage. A recent study has demonstrated that in blood cells of aging subjects, p53 may induce early pathological changes that precede the amyloidogenic cascade. However, it is not clear whether p53 participates in the local deposition of amyloid-beta peptide (Aβ) in the nerve tissue of normal aging subjects. Therefore, in the present study, we analyse the distribution of both (Aβ and p53) proteins in the cerebellum of individuals without any history of dementia or other neurological illness who died suddenly in traffic accidents. We found that in the subjects at the beginning of their aging process (60-65 years of age) Aβ deposits were localized in subependymal areas of the cerebellar cortex and such deposits were not linked to the presence of p53 in the nerve tissue. In groups of subjects over 65 years of age, numerous Aβ diffuse plaques were scattered throughout the cerebellar cortex. In these subjects, p53 protein was detected in the cytoplasm or in the nucleus of the cerebellar nerve cells. All the results lead to the conclusion that in nerve tissue p53 participates in the process of neurodegeneration and then it is involved in the deposition of A in the nerve tissue.
AbstractList Protein p53 is known to induce the cell cycle arrest and apoptosis in response to a variety of cellular distress signals and DNA damage. A recent study has demonstrated that in blood cells of aging subjects, p53 may induce early pathological changes that precede the amyloidogenic cascade. However, it is not clear whether p53 participates in the local deposition of amyloid-beta peptide (Aβ) in the nerve tissue of normal aging subjects. Therefore, in the present study, we analyse the distribution of both (Aβ and p53) proteins in the cerebellum of individuals without any history of dementia or other neurological illness who died suddenly in traffic accidents. We found that in the subjects at the beginning of their aging process (60-65 years of age) Aβ deposits were localized in subependymal areas of the cerebellar cortex and such deposits were not linked to the presence of p53 in the nerve tissue. In groups of subjects over 65 years of age, numerous Aβ diffuse plaques were scattered throughout the cerebellar cortex. In these subjects, p53 protein was detected in the cytoplasm or in the nucleus of the cerebellar nerve cells. All the results lead to the conclusion that in nerve tissue p53 participates in the process of neurodegeneration and then it is involved in the deposition of A in the nerve tissue.
Author Księżopolska-Orłowska, Krystyna
Szukiewicz, Dariusz
Maślińska, Danuta
Maśliński, Sławomir
Laure-Kamionowska, Milena
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Issue 2
Keywords neurodegeneration
amyloid-beta (Aβ) deposits
aging
cerebellum
p53
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Snippet Protein p53 is known to induce the cell cycle arrest and apoptosis in response to a variety of cellular distress signals and DNA damage. A recent study has...
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StartPage 161
SubjectTerms Aged
Aged, 80 and over
aging
Aging - metabolism
Aging - pathology
Amyloid beta-Protein Precursor - metabolism
amyloid-beta (Aβ) deposits
cerebellum
Cerebellum - metabolism
Cerebellum - pathology
Humans
Middle Aged
neurodegeneration
p53
Plaque, Amyloid - pathology
Tumor Suppressor Protein p53 - metabolism
Title Commitment of protein p53 and amyloid-beta peptide (Aβ) in aging of human cerebellum
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