Apoptosis and autophagy are key physiologic processes essentially required for cellular homeostasis. Irreparable genomic damage or severe oxidative stress triggers the apoptosis process to clear the damaged cell from the tissue. Apoptosis plays a homeostatic function in sustaining neural and brain health. Apoptosis is well characterized by its distinct morphology that includes membrane blebbing, cytoskeletal collapse, cytoplasmic condensation/fragmentation, pyknosis of nucleus, chromatin condensation/fragmentation, and apoptotic bodies (membrane-enveloped) formation that are eventually eliminated by macrophages or adjacent cells by phagocytosis. While autophagy sustains neural and brain health by targeting the aging cytosolic proteins and injured organelles. Autophagy comprises a series of events that includes the formation and elongation of double-membrane, vesicle maturation, and eventual elimination of targeted material by the lysosome. Being the specialized post-mitotic cells, neurons inherently rely on high mitochondria output given to their greater bioenergetic need, thus the role of mitochondrial quality control (QC) mechanisms such as mitophagy is vital and thus plays a critical role in sustaining neuronal health and function. Emerging evidence revealed that the cellular process of apoptosis, autophagy, and mitophagy are impaired in Alzheimer’s disease (AD), though the etiology and molecular trigger of these mechanisms are elusive. Declined physiological functions in the aging population were speculated to be the result of altered metabolic and molecular pathways that were seen intermingled among the apoptosis, autophagy, and mitophagy processes. Taking on the impaired oxidative stress, mitochondria, and lysosomes pathways in the neurodegenerative diseases, in this Research Topic, we aim to consolidate the evolving cellular and molecular knowledge of the intricated apoptosis, autophagy, and mitophagy processes and their dysfunctions in Alzheimer's disease by shedding light on their emerging links and translational importance.
We welcome researchers working in these domains to contribute with the Original Research, Review, Methods, and Perspective/cohort reports, Hypothesis/Theory, Opinions, and Commentaries. Besides the exciting research in the specialized AD domain, we welcome submissions highlighting the emerging cellular and molecular processes of apoptosis, autophagy, and mitophagy in the brain disease mechanisms and its functional importance in the context of AD and other related neurodegenerative diseases. We target, yet not limited to AD, to cover the following non-exhaustive list of sub-themes:
1. Molecular cues and processes promoting neural cell death/apoptosis in Alzheimer's disease.
2. Cellular and molecular factors impairing the autophagy process in AD and their clinical significance.
3. Molecular bases of impaired oxidative stress, mitochondria, and lysosomes pathways in the neurodegenerative diseases
4. Role of mitophagy defects and accumulation of damaged/dysfunctional mitochondria in neurodegenerative disease progression
5. Involvement of impaired mitochondrial function and associated bioenergetic deficit, intracellular Ca2+ imbalance, and oxidative stress processes in the synaptic dysfunction, cognitive- and memory loss.
6. Emerging overlaps and association in autophagy and mitophagy in brain disease mechanisms
7. Manipulation and re-wiring of apoptosis, autophagy, and mitophagy processes to prevent neurodegenerative diseases
8. Present outlook and crossroad of apoptosis, autophagy, and mitophagy processes in brain disease mechanisms and neuro-pathologies.
Apoptosis and autophagy are key physiologic processes essentially required for cellular homeostasis. Irreparable genomic damage or severe oxidative stress triggers the apoptosis process to clear the damaged cell from the tissue. Apoptosis plays a homeostatic function in sustaining neural and brain health. Apoptosis is well characterized by its distinct morphology that includes membrane blebbing, cytoskeletal collapse, cytoplasmic condensation/fragmentation, pyknosis of nucleus, chromatin condensation/fragmentation, and apoptotic bodies (membrane-enveloped) formation that are eventually eliminated by macrophages or adjacent cells by phagocytosis. While autophagy sustains neural and brain health by targeting the aging cytosolic proteins and injured organelles. Autophagy comprises a series of events that includes the formation and elongation of double-membrane, vesicle maturation, and eventual elimination of targeted material by the lysosome. Being the specialized post-mitotic cells, neurons inherently rely on high mitochondria output given to their greater bioenergetic need, thus the role of mitochondrial quality control (QC) mechanisms such as mitophagy is vital and thus plays a critical role in sustaining neuronal health and function. Emerging evidence revealed that the cellular process of apoptosis, autophagy, and mitophagy are impaired in Alzheimer’s disease (AD), though the etiology and molecular trigger of these mechanisms are elusive. Declined physiological functions in the aging population were speculated to be the result of altered metabolic and molecular pathways that were seen intermingled among the apoptosis, autophagy, and mitophagy processes. Taking on the impaired oxidative stress, mitochondria, and lysosomes pathways in the neurodegenerative diseases, in this Research Topic, we aim to consolidate the evolving cellular and molecular knowledge of the intricated apoptosis, autophagy, and mitophagy processes and their dysfunctions in Alzheimer's disease by shedding light on their emerging links and translational importance.
We welcome researchers working in these domains to contribute with the Original Research, Review, Methods, and Perspective/cohort reports, Hypothesis/Theory, Opinions, and Commentaries. Besides the exciting research in the specialized AD domain, we welcome submissions highlighting the emerging cellular and molecular processes of apoptosis, autophagy, and mitophagy in the brain disease mechanisms and its functional importance in the context of AD and other related neurodegenerative diseases. We target, yet not limited to AD, to cover the following non-exhaustive list of sub-themes:
1. Molecular cues and processes promoting neural cell death/apoptosis in Alzheimer's disease.
2. Cellular and molecular factors impairing the autophagy process in AD and their clinical significance.
3. Molecular bases of impaired oxidative stress, mitochondria, and lysosomes pathways in the neurodegenerative diseases
4. Role of mitophagy defects and accumulation of damaged/dysfunctional mitochondria in neurodegenerative disease progression
5. Involvement of impaired mitochondrial function and associated bioenergetic deficit, intracellular Ca2+ imbalance, and oxidative stress processes in the synaptic dysfunction, cognitive- and memory loss.
6. Emerging overlaps and association in autophagy and mitophagy in brain disease mechanisms
7. Manipulation and re-wiring of apoptosis, autophagy, and mitophagy processes to prevent neurodegenerative diseases
8. Present outlook and crossroad of apoptosis, autophagy, and mitophagy processes in brain disease mechanisms and neuro-pathologies.
