About this Research Topic
Alzheimer's disease (AD) and Parkinson's disease (PD) are the most prevalent neurodegenerative disorders, posing significant health burdens globally. Both diseases have complex etiologies where genetics play a crucial role. Understanding the genetic basis of AD and PD is essential for developing targeted therapies and preventive strategies.
Both diseases are characterized by progressive neuronal loss, yet they manifest distinct clinical symptoms and pathologies. AD primarily affects cognitive function, leading to memory loss, confusion, and behavioral changes. The hallmark pathological features of AD include the accumulation of amyloid-beta plaques and tau neurofibrillary tangles within the brain. These protein aggregates disrupt neuronal communication and ultimately result in cell death.
PD, on the other hand, primarily affects motor function, causing symptoms such as tremors, rigidity, bradykinesia, and postural instability. The defining pathological feature of PD is the presence of Lewy bodies, which are abnormal aggregates of alpha-synuclein protein, within dopaminergic neurons of the substantia nigra. The loss of these dopamine-producing neurons leads to the characteristic motor deficits seen in PD patients.
Despite their differences, AD and PD share several common mechanisms, including mitochondrial dysfunction, oxidative stress, neuroinflammation, and impaired protein degradation pathways. Genetic factors play a significant role in both diseases, with mutations in genes such as APP, PSEN1, and APOE linked to familial AD, and mutations in SNCA, LRRK2, and PARK2 associated with familial PD. Additionally, genome-wide association studies have identified numerous risk loci for both sporadic AD and PD, highlighting the complex interplay between genetic susceptibility and environmental influences.
Recent advancements in genetic technologies, such as next-generation sequencing and CRISPR-Cas9 are paving the way for developing novel diagnostic markers and therapeutic targets for these diseases. Therefore, this Research Topic aims to provide a comprehensive collection of research that focus on understanding of the genetic underpinnings of AD and PD. We welcome Original Research Articles, Reviews, Mini-Reviews, Systematic Reviews, Perspectives, Commentaries, Data notes, and technical notes, but are not limited to the following:
• Investigate the role of newly identified genetic variants from genome-wide association studies (GWAS) in AD and PD pathogenesis.
• Develop and validate novel biomarkers for early diagnosis, progression monitoring, and therapeutic response in AD and PD.
• Examine the role of neuroinflammation and the immune response in the progression of AD and PD, focusing on microglia and astrocytes.
• Analyze how environmental factors, such as toxins or lifestyle choices, interact with genetic predispositions to influence the onset and progression of AD and PD.
• Implement precision medicine strategies by integrating genetic, epigenetic, and phenotypic data to personalize treatment plans for AD and PD patients.
Both diseases are characterized by progressive neuronal loss, yet they manifest distinct clinical symptoms and pathologies. AD primarily affects cognitive function, leading to memory loss, confusion, and behavioral changes. The hallmark pathological features of AD include the accumulation of amyloid-beta plaques and tau neurofibrillary tangles within the brain. These protein aggregates disrupt neuronal communication and ultimately result in cell death.
PD, on the other hand, primarily affects motor function, causing symptoms such as tremors, rigidity, bradykinesia, and postural instability. The defining pathological feature of PD is the presence of Lewy bodies, which are abnormal aggregates of alpha-synuclein protein, within dopaminergic neurons of the substantia nigra. The loss of these dopamine-producing neurons leads to the characteristic motor deficits seen in PD patients.
Despite their differences, AD and PD share several common mechanisms, including mitochondrial dysfunction, oxidative stress, neuroinflammation, and impaired protein degradation pathways. Genetic factors play a significant role in both diseases, with mutations in genes such as APP, PSEN1, and APOE linked to familial AD, and mutations in SNCA, LRRK2, and PARK2 associated with familial PD. Additionally, genome-wide association studies have identified numerous risk loci for both sporadic AD and PD, highlighting the complex interplay between genetic susceptibility and environmental influences.
Recent advancements in genetic technologies, such as next-generation sequencing and CRISPR-Cas9 are paving the way for developing novel diagnostic markers and therapeutic targets for these diseases. Therefore, this Research Topic aims to provide a comprehensive collection of research that focus on understanding of the genetic underpinnings of AD and PD. We welcome Original Research Articles, Reviews, Mini-Reviews, Systematic Reviews, Perspectives, Commentaries, Data notes, and technical notes, but are not limited to the following:
• Investigate the role of newly identified genetic variants from genome-wide association studies (GWAS) in AD and PD pathogenesis.
• Develop and validate novel biomarkers for early diagnosis, progression monitoring, and therapeutic response in AD and PD.
• Examine the role of neuroinflammation and the immune response in the progression of AD and PD, focusing on microglia and astrocytes.
• Analyze how environmental factors, such as toxins or lifestyle choices, interact with genetic predispositions to influence the onset and progression of AD and PD.
• Implement precision medicine strategies by integrating genetic, epigenetic, and phenotypic data to personalize treatment plans for AD and PD patients.
Keywords: Alzheimer's disease, Parkinson's disease, Cognitive Function, Brain, Genetics
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