Effects of low molecular weight glycosaminoglycans in amyloid beta-induced models of Alzheimer's disease

Alzheimer's Disease (AD) is a progressive neurodegenerative disease mainly affecting the elderly population. Current treatment modalities alleviate the symptoms while not affecting the underlying causes of the disease. Future treatments are needed which prevent the underlying disease etiology. Amyloid beta (Aβ) deposited in the senile plaques is one of two neuropathological hallmarks of AD. Hyperphosphorylated and/or conformationally-altered tau protein forms neurofibrillary tangles (NFTs), which is the other neuropathological hallmark of AD. Previous research has shown a strong link between Aβ deposition and tau pathology, suggesting Aβ deposition may induce both neuropathological hallmarks. Subsequently, low molecular weight heparins have been shown to prevent Aβ deposition. However these studies did not investigate the subsequent effects of low molecular weight heparin treatment on tau pathology. Hence, this dissertation studied the treatment effects of low molecular weight heparins on Aβ-induced tau pathology using wild-type rat and transgenic tau mouse models, as well as cell culture and in vitro techniques. The results of this dissertation suggest low molecular weight heparin treatment may be beneficial in preventing the early neuropathology associated with AD.