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The most common secondary damage is ipsilateral thalamic degeneration after cerebral infarction, including axonal degeneration, neuronal loss, gliosis, -amyloid (A) deposits, and hyperphosphorylation of Tau protein (152, 153)

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These include genetic defects affecting -cell function or insulin action, as well as diseases of the exocrine pancreas such as cystic fibrosis and pancreatitis that can contribute to the development of diabetes