TY - JOUR
T1 - Reappraisal of the Concept of Accelerated Aging in Neurodegeneration and Beyond
AU - Statsenko, Yauhen
AU - Kuznetsov, Nik V.
AU - Morozova, Daria
AU - Liaonchyk, Katsiaryna
AU - Simiyu, Gillian Lylian
AU - Smetanina, Darya
AU - Kashapov, Aidar
AU - Meribout, Sarah
AU - Gorkom, Klaus Neidl Van
AU - Hamoudi, Rifat
AU - Ismail, Fatima
AU - Ansari, Suraiya Anjum
AU - Emerald, Bright Starling
AU - Ljubisavljevic, Milos
N1 - Publisher Copyright:
© 2023 by the authors.
PY - 2023/10
Y1 - 2023/10
N2 - Background: Genetic and epigenetic changes, oxidative stress and inflammation influence the rate of aging, which diseases, lifestyle and environmental factors can further accelerate. In accelerated aging (AA), the biological age exceeds the chronological age. Objective: The objective of this study is to reappraise the AA concept critically, considering its weaknesses and limitations. Methods: We reviewed more than 300 recent articles dealing with the physiology of brain aging and neurodegeneration pathophysiology. Results: (1) Application of the AA concept to individual organs outside the brain is challenging as organs of different systems age at different rates. (2) There is a need to consider the deceleration of aging due to the potential use of the individual structure–functional reserves. The latter can be restored by pharmacological and/or cognitive therapy, environment, etc. (3) The AA concept lacks both standardised terminology and methodology. (4) Changes in specific molecular biomarkers (MBM) reflect aging-related processes; however, numerous MBM candidates should be validated to consolidate the AA theory. (5) The exact nature of many potential causal factors, biological outcomes and interactions between the former and the latter remain largely unclear. Conclusions: Although AA is commonly recognised as a perspective theory, it still suffers from a number of gaps and limitations that assume the necessity for an updated AA concept.
AB - Background: Genetic and epigenetic changes, oxidative stress and inflammation influence the rate of aging, which diseases, lifestyle and environmental factors can further accelerate. In accelerated aging (AA), the biological age exceeds the chronological age. Objective: The objective of this study is to reappraise the AA concept critically, considering its weaknesses and limitations. Methods: We reviewed more than 300 recent articles dealing with the physiology of brain aging and neurodegeneration pathophysiology. Results: (1) Application of the AA concept to individual organs outside the brain is challenging as organs of different systems age at different rates. (2) There is a need to consider the deceleration of aging due to the potential use of the individual structure–functional reserves. The latter can be restored by pharmacological and/or cognitive therapy, environment, etc. (3) The AA concept lacks both standardised terminology and methodology. (4) Changes in specific molecular biomarkers (MBM) reflect aging-related processes; however, numerous MBM candidates should be validated to consolidate the AA theory. (5) The exact nature of many potential causal factors, biological outcomes and interactions between the former and the latter remain largely unclear. Conclusions: Although AA is commonly recognised as a perspective theory, it still suffers from a number of gaps and limitations that assume the necessity for an updated AA concept.
KW - accelerated aging
KW - aging
KW - biological clocks
KW - brain aging
KW - epigenetics
KW - molecular biomarkers
KW - neurodegeneration
KW - rejuvenation
UR - http://www.scopus.com/inward/record.url?scp=85175097815&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85175097815&partnerID=8YFLogxK
U2 - 10.3390/cells12202451
DO - 10.3390/cells12202451
M3 - Review article
C2 - 37887295
AN - SCOPUS:85175097815
SN - 2073-4409
VL - 12
JO - Cells
JF - Cells
IS - 20
M1 - 2451
ER -