Alzheimer's disease is a highly pleiotropic disease which typically manifests in late life despite an individual harboring genetic risk from birth. While interactions of the environment with genetic risk factors over a course of an individual’s lifetime are thought to alter an individual’s risk of dementia, there is increasing evidence that AD-relevant genetic risk factors such as APP and PS1 can directly impact neurogenesis, with neuroanatomical changes observed in children harboring the APOE4 risk gene. Epidemiological studies further suggest that factors such as prenatal infections and early life adversity may increase an individual's susceptibility to AD in later life. Here we propose that genetic and environmental risk factors in-utero may alter the developing brain and neural circuitry to confer AD-risk from the earliest stages of life and propose this could underlie different dementia subtypes. We contrast this with the hypothesis that developmental pathways are aberrantly reactivated during later-life.
Understanding how risk may be conferred from the earliest stages of life is essential for an early therapeutic intervention. Can we minimize the risk of AD from pregnancy and do risk factors during development contribute to differing dementia subtypes? This is a controversial hypothesis as pathological changes in the brain are only evidenced decades later.
The purpose of this Research Topic of articles is to collate the evidence and opinions for and against a developmental origin of AD and dementia subtypes, from a multi-disciplinary perspective. This would comprise a short commentary/opinion or short review articles from developmental neurobiologists, dementia researchers, clinicians and epidemiologists assessing whether AD can be viewed as a neurodevelopmental disease, or if it’s a consequence of the aberrant reactivation of developmental pathways. We propose how future studies should best tackle this hypothesis and further discuss the therapeutic implications and practicalities of reducing AD-risk from pregnancy and during childhood.
Keywords:
Alzheimer's Disease. neurodevelopment, risk, early life
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
Alzheimer's disease is a highly pleiotropic disease which typically manifests in late life despite an individual harboring genetic risk from birth. While interactions of the environment with genetic risk factors over a course of an individual’s lifetime are thought to alter an individual’s risk of dementia, there is increasing evidence that AD-relevant genetic risk factors such as APP and PS1 can directly impact neurogenesis, with neuroanatomical changes observed in children harboring the APOE4 risk gene. Epidemiological studies further suggest that factors such as prenatal infections and early life adversity may increase an individual's susceptibility to AD in later life. Here we propose that genetic and environmental risk factors in-utero may alter the developing brain and neural circuitry to confer AD-risk from the earliest stages of life and propose this could underlie different dementia subtypes. We contrast this with the hypothesis that developmental pathways are aberrantly reactivated during later-life.
Understanding how risk may be conferred from the earliest stages of life is essential for an early therapeutic intervention. Can we minimize the risk of AD from pregnancy and do risk factors during development contribute to differing dementia subtypes? This is a controversial hypothesis as pathological changes in the brain are only evidenced decades later.
The purpose of this Research Topic of articles is to collate the evidence and opinions for and against a developmental origin of AD and dementia subtypes, from a multi-disciplinary perspective. This would comprise a short commentary/opinion or short review articles from developmental neurobiologists, dementia researchers, clinicians and epidemiologists assessing whether AD can be viewed as a neurodevelopmental disease, or if it’s a consequence of the aberrant reactivation of developmental pathways. We propose how future studies should best tackle this hypothesis and further discuss the therapeutic implications and practicalities of reducing AD-risk from pregnancy and during childhood.
Keywords:
Alzheimer's Disease. neurodevelopment, risk, early life
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.