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Dendrite
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== Overview of Clinical Implications of Dendrite Dysfunction == Dendrite dysfunction and alterations in dendrite morphology may contribute to many neuropathies and diseases. Changes in dendrite morphology may include alterations in branching patterns, fragmentation, loss of branching, and alterations in spine morphology and number. Such abnormalities contribute to a wide range of [[Neurodevelopmental disorder|neurodevelopmental]] and [[Neurodegenerative disease|neurodegenerative]] disorders such as autism spectrum disorders (ASDs), [[schizophrenia]], [[down syndrome]], [[fragile X syndrome]], [[Alzheimer's disease]] (AD), and more. For example, subjects with ASD were observed to have reduced dendrite branching in the CA1 and CA4 regions of the [[hippocampus]], in addition to increased spine density. In [[Rett syndrome|Rett Syndrome]], researchers have observed less dendrite branching in the [[Basal dendrite|basal dendrites]] of the [[motor cortex]] and [[subiculum]]. In schizophrenic patients, reduced dendritic arbor (the tree-like network of dendrites) and spine density were observed. In addition to psychological and neurodevelopmental disorders, dendrite dysfunction has also been seen to have implications in onset of neurodegenerative diseases such as Alzheimer's. Alzheimer's patients have been observed to have significant changes in dendritic arbor, as well as smaller dendrite lengths in the apical and basal trees of the CA1a and CA1b areas of the hippocampus. As such, there is much continuous research exploring the effects of dysfunction in dendritic branching and morphology, and scientists continue to expand their study in this field to better understand the basis of various neurological disorders.<ref>{{Cite journal |last=Kulkarni |first=Vaishali A. |last2=Firestein |first2=Bonnie L. |date=2012-05-01 |title=The dendritic tree and brain disorders |url=https://www.sciencedirect.com/science/article/abs/pii/S1044743112000450?via=ihub |journal=Molecular and Cellular Neuroscience |volume=50 |issue=1 |pages=10β20 |doi=10.1016/j.mcn.2012.03.005 |issn=1044-7431|url-access=subscription }}</ref>
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