Jornal de Patologia Médica e Cirúrgica
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Abstrato

Synaptic Dysfunction and Neuro Inflammation Intracellular Effectors in Alzheimer's and other Neurodegenerative Disorders

Akari Andro*

Dynamic processes controlled by regulators of plasticity or morphogenesis of pre- and postsynaptic compartments sustain synaptic function. Around the time of disease initiation in neurodegenerative disorders, including Alzheimer's disease (AD), synaptic dysfunction frequently precedes neuronal loss and dysregulated microglia induces prolonged neuro inflammation with serious clinical symptoms. While astrocyte-derived apolipoprotein E4 (ApoE4) impaired amyloid beta (Aβ) clearance has been considered to be the key contributor to sporadic AD, it has been shown that intracellular effectors, such as cell-adhesion regulatory proteins or lipophilic mediators, regulate synaptic homeostasis and are further involved in controlling chronic inflammatory dissemination during neurodegenerative times. The proteins of the catenin family, such as β-catenin and p120 catenin, control the trafficking of cadherin and cytoskeletal rearrangement. The signalling of aberrant catenin has been shown to play a role in neuronal dysfunction seen in models of AD or Parkinson's disease (PD) with irregular amyloid precursor protein (APP) or oxidative vulnerability processing.