Abstract
Alzheimer’s disease (AD) as a progressive and fatal neurodegenerative disease represents a huge unmet need for treatment. The low efficacy of current treatment methods is not only due to low drug potency but also due to the presence of various obstacles in the delivery routes. One of the main barriers is the blood–brain barrier. The increasing prevalence of AD and the low efficacy of current therapies have increased the amount of research on unraveling of disease pathways and development of treatment strategies. One of the interesting areas for the latter subject is biomaterials and their applications. This interest originates from the fact that biomaterials are very useful for the delivery of therapeutic agents, such as drugs, proteins, and/or cells, in order to treat diseases and regenerate tissues. Recently, manufacturing of nano-sized delivery systems has increased the efficacy and delivery potential of biomaterials. In this article, we review the latest developments with regard to the use of biomaterials for the treatment of AD, including nanoparticles and liposomes for delivery of therapeutic compounds and scaffolds for cell delivery strategies.
Highlights
Neurological diseases, such as frontotemporal dementia, stroke-induced vascular dementia, and Alzheimer’s disease (AD), are characterized by the impairment of memory and cognitive functions (Han et al, 2015)
This indicates that the current treatment of AD with Food and Drug Administration (FDA)-approved drugs may benefit from controlled release strategies (Zhang et al, 2007)
Hippocampal transplantation of neural stem cells (NSC) with RADA16-YIGSR scaffolds improved spatial learning and memory in a rat model of AD. This was accompanied by increased neuronal survival and differentiation, less apoptosis, recovery of synaptic function, and increased neurotrophin levels (Cui et al, 2016). These results indicate that the use of NSC together with biomaterials is a promising approach for the clinical treatment of AD
Summary
Neurological diseases, such as frontotemporal dementia, stroke-induced vascular dementia, and Alzheimer’s disease (AD), are characterized by the impairment of memory and cognitive functions (Han et al, 2015). Alzheimer’s disease can be classified as familial AD or sporadic AD, while they share clinical and pathological features, including progressive cognitive impairment, plaque deposits in the brain, axonal transport defects, synapse loss, and selective neuronal death. The presence of NFTs and Aβ plaques in the brain causes shrinkage pressure, which leads to nerve cell apoptosis. Based on studies on familial AD, mutations were only seen in APP and presenilin genes (PS1 and PS2), and no mutations were reported for tau protein This finding suggests that hyperphosphorylation and aggregation of tau protein in the form of NFTs result from the direct effect of Aβ peptides on tau protein (Ranka et al, 2002). As amyloid plaque formation is a rather late process (Orive et al, 2009), more insight in the formation of Aβ peptide is needed in order to get a comprehensive understanding of the etiology of this disease
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