Biological clock changes in the aging brain
-
1
University of Verona, Department of Morphological and Biomedical Sciences, Italy
-
2
Karolinska Institutet, Department of Neuroscience, Faculty of Health,Medicine and Life Sciences, Sweden
Aging “is a privilege and a societal achievement”, as stated by the WHO (www.who.int/ageing), and the general increase of human life expectancy is rapidly changing demographic figures worldwide. A 2007 report of the United Nations Population Division (UNPD) predicts that the world’s population is set to exceed nine billion people by 2050 and almost a quarter of them will be over 60 (number of people over 60 predicted to soar from 673 million in 2005 to two billion by 2050). WHO also states that “today about two-thirds of all older people are living in the developing world; by 2025, it will be 75%”. This raises urgent issues related not only to aging as risk factor for diseases (and neurological diseases in particular), but also to “healthy” aging, a puzzling aspect of which is represented by the frequent dysregulation of endogenous biological rhythms. For example, the sleep pattern and its alternation with wakefulness are typically disrupted in the elderly, with reduction in sleep efficiency, excessive daytime sleepiness and increased napping. These alterations notably affect the quality of life of elderly individuals with considerable societal impact. Many of the changes documented in rhythm regulation in elderly humans, which have been ascribed to impaired circadian regulation, also occur in aged laboratory rodents. Interestingly, a wealth of data has indicated that normal aging is hallmarked by low-grade chronic inflammatory activity, with increased production of proinflammatory cytokines peripherally and in the brain and decreased anti-inflammatory mediators. Information on immune-regulatory mechanisms in the suprachiasmatic nucleus of the hypothalamus (SCN), the main circadian pacemaker in the mammalian brain, is still limited, but in the last years, a number of reports have pointed out that SCN function is affected by immune-related challenges. In this context, we have investigated molecular and cellular changes in the SCN of old mice, not only in normal conditions but also in response to intracerebroventricular administration of proinflammatory cytokines. We have thus documented in the old mouse SCN aging-related increases of the mRNA expression of the astrocyte marker GFAP and the microglial marker CD11b, as well as aging-related changes of glial cells, and an exaggerated response of such cells to cytokine exposure. We have also investigated in mice whether the expression of clock genes varies in the SCN and peripheral organs (heart and liver) during aging. In the latter study, we detected changes suggesting an age-related impairment in the multioscillatory system linking the brain master pacemaker with peripheral oscillators. Altogether, our findings point out remarkable changes of brain clock mechanisms and function during senescence.
Conference:
3rd Mediterranean Conference of Neuroscience , Alexandria, Egypt, 13 Dec - 16 Dec, 2009.
Presentation Type:
Oral Presentation
Topic:
Symposium 25 – From Circadian Clock to Human Health
Citation:
Bentivoglio
M,
Palomba
M,
Bonaconsa
M,
Deng
XH,
Nygard
M,
Xu
YZ,
Bertini
G and
Kristensson
K
(2009). Biological clock changes in the aging brain.
Front. Neurosci.
Conference Abstract:
3rd Mediterranean Conference of Neuroscience .
doi: 10.3389/conf.neuro.01.2009.16.098
Copyright:
The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers.
They are made available through the Frontiers publishing platform as a service to conference organizers and presenters.
The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated.
Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed.
For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions.
Received:
23 Nov 2009;
Published Online:
23 Nov 2009.
*
Correspondence:
Marina Bentivoglio, University of Verona, Department of Morphological and Biomedical Sciences, Verona, Italy, marina.bentivoglio@univr.it