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Titlebook: Behavioral Neurobiology of Huntington‘s Disease and Parkinson‘s Disease; Hoa Huu Phuc Nguyen,M. Angela Cenci Book 2015 The Editor(s) (if a

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發(fā)表于 2025-3-23 11:38:10 | 只看該作者
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發(fā)表于 2025-3-23 17:46:43 | 只看該作者
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發(fā)表于 2025-3-23 21:32:47 | 只看該作者
Comparing Results to Regression Resultsential neuronal loss in distinct brain regions. Mutant huntingtin causes late-onset neurological symptoms in patients in middle life, though the expression of mutant huntingtin is ubiquitous from early life. Thus, it is important to understand why mutant huntingtin selectively causes neuronal loss i
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發(fā)表于 2025-3-23 23:07:31 | 只看該作者
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發(fā)表于 2025-3-24 05:21:29 | 只看該作者
Setting Up Research: Complicationsmmatory processes are exacerbated in Parkinson’s disease, including glial-mediated reactions, increased expression of proinflammatory substances, and lymphocytic infiltration, particularly in the substantia nigra. Neuroinflammation is also implicated in the neurodegeneration and consequent behaviora
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發(fā)表于 2025-3-24 07:20:20 | 只看該作者
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發(fā)表于 2025-3-24 16:01:02 | 只看該作者
Comparing Results to Regression Resultsmon variation at the . genomic locus influences the risk of developing idiopathic PD. LRRK2 is a member of the ROCO protein family and contains multiple domains, including Ras-of-Complex (ROC) GTPase, kinase, and protein-protein interaction domains. In the last decade, the biochemical characterizati
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發(fā)表于 2025-3-24 19:59:49 | 只看該作者
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發(fā)表于 2025-3-25 01:55:20 | 只看該作者
Comparing Results to Regression Resultsrived induced pluripotent stem cells. We discuss how these models have contributed to understanding LRRK2 pathobiology and the advantages and limitations of each model for exploring aspects of .-associated PD.
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