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The new edition of Gene Control has been updated to include significant advances in the roles of the epigenome and regulatory RNAs in gene regulation. The chapter structure remains the same: the first part consists of pairs of chapters that explain the mechanisms involved and how they regulate gene expression, and the second part deals with specific biological processes (including diseases) and how they are controlled by genes. Coverage of methodology has been strengthened by the inclusion more explanation and diagrams.
The new edition of Gene Control has been updated to include significant advances in the roles of the epigenome and regulatory RNAs in gene regulation. The chapter structure remains the same: the first part consists of pairs of chapters that explain the mechanisms involved and how they regulate gene expression, and the second part deals with specific biological processes (including diseases) and how they are controlled by genes. Coverage of methodology has been strengthened by the inclusion more explanation and diagrams.
The substantia nigra (SN) is a midbrain dopaminergic nucleus which has a critical role in modulating motor movement and reward functions as part of the basal ganglia circuitry. Projections from the SN to the putamen, called the nigrostriatal pathway, are critically involved in the motor deficits observed in Parkinson disease.[1] These dopaminergic neural projections leave the SN via the medial forebrain bundle and forming synapses on multiple neuronal populations throughout the basal ganglia, but especially in the putamen. The basal ganglia are a grouping of interconnected subcortical nuclei that mitigate and control functions ranging from voluntary movement, cognitive planning, emotions and reward functions, and even cognition and learning. The substantia nigra is classically considered to be the primary input into the basal ganglia circuitry and a critical element to these functions. When these subcortical nuclei are damaged such as in stroke or during neurodegeneration, a multitude of neurological conditions can result, including Parkinson disease, Huntington disease, Tourette syndrome, schizophrenia, attention-deficit hyperactivity disorder, and obsessive-compulsive disorder.
Using the tyrosine hydroxylase (TH) enzyme, the rate-limiting enzyme in dopamine biosynthesis, as a marker for dopaminergic neurons, embryonic studies suggest that the dopaminergic substantia nigra neurons first form in the ventricular zone of the ventral mesencephalon during week 6.5 with migration occurring at week six.[4] By week eight the TH-positive neurons began to form neural projections of the nigrostriatal bundle. Other studies indicate that the SNpc and SNpr segregate at around week 19.[5] In rodent studies, these timelines seem to correlate with embryonic days 13 through 15 and are dependent upon the transcription factor Pitx3.[6][7][8] The PBX1 gene directly controls the Pitx3 gene expression as well as a gene involved in protection from oxidative stress, and PBX1 has been found to be less active in adult Parkinson disease patients.[9] In rodent studies, mutations in many of these genes are embryonically lethal; however, a number of genes have an association with juvenile or early-onset parkinsonism in humans, defined by the National Institute of Neurological Disorders and Stroke (NINDS) as onset before the age of 50. These include the PINK1 gene,[10] PARKIN,[11] SNCA,[12] and LRRK2.[13] Idiopathic parkinsonism typically develops late in life with a mean age of onset around 60 years with approximately 1% of that population suffering from the condition (NINDS, 2016). 153554b96e
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