2005
DOI: 10.1196/annals.1356.006
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Lunasensor, Infradian Rhythms, Telomeres, and the Chronomere Program of Aging

Abstract: According to the redusome hypothesis, the aging of an organism is determined by the shortening of chronomeres (small perichromosomal linear DNA molecules). In this paper, a presumptive role for infradian hormonal rhythms is considered. Endogenous infradian rhythms are supposed to actively interact with those hormonal shifts which are governed by an exogenous infradian gravitational lunar rhythm. As a result of this interaction, the so-called T-rhythm is formed. Peaks of T-rhythms are used as the pacemaker sign… Show more

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Cited by 21 publications
(7 citation statements)
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“…peculiar micrograins, and other morphological changes are in accordance with the phases of the moon, one can deduce that the cause of the observed changes is also based on the lunar influence. This is consistent with the prediction of the lunasensor hypothesis about the role of the pineal gland as a peculiar gravisensor [9,10].…”
Section: Discussionsupporting
confidence: 90%
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“…peculiar micrograins, and other morphological changes are in accordance with the phases of the moon, one can deduce that the cause of the observed changes is also based on the lunar influence. This is consistent with the prediction of the lunasensor hypothesis about the role of the pineal gland as a peculiar gravisensor [9,10].…”
Section: Discussionsupporting
confidence: 90%
“…However, the lifelong clock persists ticking even after physiological maturation of the body has been completed. And just this could be the pivotal cause that gradually leads the organism to aging [9,10]. According to this hypothesis, pinealocytes should change their secretory activity in the new and full moon, period ically modifying some of their own morphological fea tures and other properties of the body as well, by exposing them to periodic changes in the profile of the neuroen docrine activity and secretion.…”
mentioning
confidence: 97%
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“…This structure prevents chromosome ends from being recognized as DNA double-strand breaks and therefore being processed by the DNA repair machinery. Due to the inability of DNA polymerases to completely replicate linear genomes – the so-called “end-replication problem” (Watson, 1972; Olovnikov, 2005) – cells undergo telomere shortening at every replication round. The loss of terminal DNA is counteracted by the activity of the telomerase enzyme, which adds de novo telomeric repeats to the G-rich 3′-overhang (Blackburn, 2005).…”
Section: Introductionmentioning
confidence: 99%
“…Loss of telomeric protection can lead to the formation of end-to-end fusions, which directly disrupt the correct structure at telomere termini [5]. In addition to the inhibition of inappropriate repair responses, fusions or recombinations, telomeres need to be fully replicated by the action of telomerase to prevent end-replication problem [6], [7], [8], [9]. In S. cerevisiae , telomerase RNA and reverse transcriptase are encoded by EST2 and TLC1 , respectively.…”
Section: Introductionmentioning
confidence: 99%