With the rapid increase of the average human life span, age-related memory loss has become a more obvious phenomenon, affecting millions of healthy individuals. Age-associated memory impairment is a consequence of normal aging initially manifested as a benign memory deficit that can progressively lead to devastating forgetfulness and Alzheimer’s-like phenotypes. In the past few years, with the use of state-of-the-art technologies, several advances have been made in the neurobiology of aging, implicating metabolism, nutrition, genetics, epigenetics and physical exercise as factors that can reverse age-related phenotypes in mice and humans.
Despite the plethora of interventions in the aging field, very little is known about why certain memory functions deteriorate in some healthy individuals, and more importantly, what are the cell type-specific molecular processes and neural circuits responsible for this age-related dysfunction. Recent advances in the aging field demonstrate that aging can be reversed with a variety of novel interventions such as blood-derived factors, hormones, perturbations of the immune system, and senolytic drugs, with promising results in mouse models and in pilot preclinical studies. Therefore, it will be of great interest to elucidate the cell types that are primarily affected by these interventions along with the key signalling pathways. Another scope of this Research Topic will be to bring to light studies that have established new animal models related to aging that employ and adapt breakthrough techniques to better approach the above questions.
The scope of the current Research Topic is to cover promising, recent, and novel research trends in the aging field. Areas to be covered in this Research Topic may include, but are not limited to:
• Stem Cell rejuvenation and neurogenesis
• Cell types susceptible to aging
• Signaling cascades perturbed in aging
• Novel therapeutics (blood-born factors, senolytics and metabolism)
• Model organisms to study aging
With the rapid increase of the average human life span, age-related memory loss has become a more obvious phenomenon, affecting millions of healthy individuals. Age-associated memory impairment is a consequence of normal aging initially manifested as a benign memory deficit that can progressively lead to devastating forgetfulness and Alzheimer’s-like phenotypes. In the past few years, with the use of state-of-the-art technologies, several advances have been made in the neurobiology of aging, implicating metabolism, nutrition, genetics, epigenetics and physical exercise as factors that can reverse age-related phenotypes in mice and humans.
Despite the plethora of interventions in the aging field, very little is known about why certain memory functions deteriorate in some healthy individuals, and more importantly, what are the cell type-specific molecular processes and neural circuits responsible for this age-related dysfunction. Recent advances in the aging field demonstrate that aging can be reversed with a variety of novel interventions such as blood-derived factors, hormones, perturbations of the immune system, and senolytic drugs, with promising results in mouse models and in pilot preclinical studies. Therefore, it will be of great interest to elucidate the cell types that are primarily affected by these interventions along with the key signalling pathways. Another scope of this Research Topic will be to bring to light studies that have established new animal models related to aging that employ and adapt breakthrough techniques to better approach the above questions.
The scope of the current Research Topic is to cover promising, recent, and novel research trends in the aging field. Areas to be covered in this Research Topic may include, but are not limited to:
• Stem Cell rejuvenation and neurogenesis
• Cell types susceptible to aging
• Signaling cascades perturbed in aging
• Novel therapeutics (blood-born factors, senolytics and metabolism)
• Model organisms to study aging