{"id":4584,"date":"2016-03-11T15:06:46","date_gmt":"2016-03-11T14:06:46","guid":{"rendered":"http:\/\/m3.dti.supsi.ch\/?page_id=4584"},"modified":"2020-12-29T13:39:31","modified_gmt":"2020-12-29T12:39:31","slug":"4584-2","status":"publish","type":"page","link":"https:\/\/m3.dti.supsi.ch\/index.php\/projects\/4584-2\/","title":{"rendered":"Amyloid Beta Aggregation Mechanism"},"content":{"rendered":"

Alzheimer\u2019s disease (AD) is a highly debilitating pathological condition directly related to the abnormal aggregation of misfolded amyloidogenic proteins. The amyloid hypothesis proposes amyloid \u03b2 (A\u03b2) peptide as the main cause of the AD. The neurodegenerative disorders arise from the abnormal protein aggregation in the nervous tissue leading to intracellular inclusions or extracellular aggregates in specific brain areas. A feasible strategy to prevent the resulting neurodegeneration is based on the development of anti-amyloid molecules, i.e., those capable of preventing the generation of toxic aggregates. To address this issue, it\u2019s extremely important to shed light on the molecular interactions responsible for protein aggregation. Despite substantial research efforts in this field, the fundamental mechanisms of protein misfolding and aggregation mechanisms remain somewhat unrevealed. In this context, computational molecular modelling represents a powerful tool in connecting macroscopic experimental findings to nanoscale molecular events<\/p>\n

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Figure: Amyloid beta aggregation mechanism.<\/em><\/p>\n

Publications:<\/p>\n