About this Research Topic
Depression--the most common psychiatric disorder--occurs in one third of Alzheimer’s disease (AD) cases. Nonetheless of being highly prevalent in Alzheimer’s disease, depression is also highly predictive of incident AD, as well as constituting its common manifestations. As a consequence, dementia and depression are closely intertwined. This intricacy suggests the existence of common pathways. Therefore, the question arises as to whether one influences the other.
The overall aim of this Research Topic is to provide a global picture on how depression is linked to AD while detailing pathways underlying the depression-AD association with a multidisciplinary framework including physiology, neurobiology, neurology, neuropsychiatry, and epidemiology.
Our first specific aim will be to offer a macro view of “common” genetic factors, lifestyle factors induced by depression susceptible to modify the cerebral reserve that potentially interplay with clinical manifestations of AD, and health status factors mediating the depression-AD associations. The second specific aim will be to detail the overlap of biological underpinnings of depression and AD by considering different embedded levels of analysis. At a cellular/molecular level, we will detail the pathways linked to neuro-inflammation processes, oxidative stress and neurogenesis and assess as well the two major systems strongly implicated in depression: the hypothalamic-pituitary-adrenal (HPA) axis and the monoaminergic (serotonergic) system, including whether they interplay with amyloid cascade. At a structural level, we will review evidence of specific common brain structures impacted both by depression and AD. Finally, we will discuss potential interplay of specific physiological systems including digestive (gut microbial), circulatory and endocrine systems with central nervous system. The understanding of the mechanisms underlying depression in dementia is crucial to identify new targets and effective treatments.
Surprisingly, not too many papers related to this theme have been published, and we hope that this Research Topic will help people to investigate this exciting field.
The overall aim of this Research Topic is to provide a global picture on how depression is linked to AD while detailing pathways underlying the depression-AD association with a multidisciplinary framework including physiology, neurobiology, neurology, neuropsychiatry, and epidemiology.
Our first specific aim will be to offer a macro view of “common” genetic factors, lifestyle factors induced by depression susceptible to modify the cerebral reserve that potentially interplay with clinical manifestations of AD, and health status factors mediating the depression-AD associations. The second specific aim will be to detail the overlap of biological underpinnings of depression and AD by considering different embedded levels of analysis. At a cellular/molecular level, we will detail the pathways linked to neuro-inflammation processes, oxidative stress and neurogenesis and assess as well the two major systems strongly implicated in depression: the hypothalamic-pituitary-adrenal (HPA) axis and the monoaminergic (serotonergic) system, including whether they interplay with amyloid cascade. At a structural level, we will review evidence of specific common brain structures impacted both by depression and AD. Finally, we will discuss potential interplay of specific physiological systems including digestive (gut microbial), circulatory and endocrine systems with central nervous system. The understanding of the mechanisms underlying depression in dementia is crucial to identify new targets and effective treatments.
Surprisingly, not too many papers related to this theme have been published, and we hope that this Research Topic will help people to investigate this exciting field.
Keywords: Alzheimer's Disease, Depression, HPA Axis, Diabetes, Antidepressants, Nutrition, Cerebral Reserve, Neurotrophic Factors, Amyloid Cascade
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