Not exact matches
For Longo, it all added up: The same growth genes that
regulate aging and protect against
age - related diseases in yeast, mice, and roundworms might have an identical effect in
humans.
The big question now is whetherSIR2 - like genes also
regulate the rate of
aging in
humans.
As Huber Warner, associate director of the Biology of
Aging Program at the NationalInstitute of
Aging, says, «If we knew what
regulates life span inturtles, that might be useful in figuring out how
humans age and how tointervene.»
Potential projects include identifying common pathways that modify retinal degenerative disease from a large collection of actively maintained mouse models; determining molecular networks implicated in pathological disruption of the retinal pigment epithelium; identifying molecular pathways that
regulate postnatal ocular growth; and using mouse models to assess the pathogenic role of gene variants that increase the risk of
age - related macular degeneration as identified by
human genome - wide association studies.
Researchers at the MTA SZTAKI Big Data - Momentum (Lendület) Research Group in collaboration with the ELTE TTK Genetics Department have predicted
human proteins that
regulate ageing using the latest state - of - the - art machine learning methods.
This is bad because about 80 - 90 % of HGH (the
Human Growth Hormone that controls
aging, controls metabolism, cell growth and repair, and
regulates your lean body mass to fat ratio) is released while you sleep.
FOXO genes also interact with SIRT1, a sirtuin protein that is the
human homologue of the yeast sirtuin, silent information regulator 2 (SIR2), which assists in DNA repair and
regulates genes that undergo alteration with
age.
In
humans, both the HPA system and the autonomic nervous system show developmental changes in infancy, with the HPA axis becoming organized between 2 and 6 months of
age and the autonomic nervous system demonstrating relative stability by 6 to 12 months of
age.63 The HPA axis in particular has been shown to be highly responsive to child - caregiver interactions, with sensitive caregiving programming the HPA axis to become an effective physiological regulator of stress and insensitive caregiving promoting hyperreactive or hyporeactive HPA systems.17 Several animal models as well as
human studies also support the connection between caregiver experiences in early postnatal life and alterations of autonomic nervous system balance.63 - 65 Furthermore, children who have a history of sensitive caregiving are more likely to demonstrate optimal affective and behavioral strategies for coping with stress.66, 67 Therefore, children with histories of supportive, sensitive caregiving in early development may be better able to self -
regulate their physiological, affective, and behavioral responses to environmental stressors and, consequently, less likely to manifest disturbed HPA and autonomic reactivity that put them at risk for stress - related illnesses such as asthma.