Nanotechnology Therapy for Alzheimer′s Disease Memory Impairment Attenuation

Abstract

Currently, there is no cure for Alzheimer’s disease (AD) in humans; treatment is symptomatic only. Aging of the population, together with an unhealthy diet and lifestyle, contribute to the steady, global increase of AD patients. This increase creates significant health, societal and economical challenges even for the most developed countries. AD progresses from an asymptomatic stage to a progressively worsening cognitive impairment. The AD cognitive impairment is underpinned by progressive memory impairment, an increasing inability to recall recent events, to execute recently planned actions, and to learn. These changes prevent the AD patient from leading an independent and fulfilling life. Nanotechnology (NT) enables a new, alternative pathway for development of AD treatment interventions. At present, the NT treatments for attenuation of AD memory impairment are at the animal model stage. Over the past four years, there has been a steady increase in publications of AD animal models with a wide variety of original NT treatment interventions, able to attenuate memory impairment. NT therapy development, in animal models of AD, is faced with the twin challenges of the nature of AD, a chronic impairment, unique to human, of the tau protein and A β peptides that regulate several key physiological brain processes, and the incomplete understanding of AD′s aetiology. This paper reviews the state-of-the-art in NT based treatments for AD memory impairment in animal models and discusses the future work for translation to the successful treatment of AD cognitive impairment in human.

Nano-Theranostics Approaches and Mitochondrial Targeted Drug Delivery: Alzheimer ’s Disease Therapeutic Interventions

“…Research has shown that over expressed normal Tau and/or overexpressed mutant Tau in neurons become hyper phosphorylated, causing oxidative stress, mitochondrial dysfunction, synaptic deprivation, and neuronal damage. This was discovered using brain tissues from transgenic mouse models of Tau, APP/PS1, and 3XAD.Tg (Ribarič, 2021). Several research groups have reported oxidative damage, defective mitochondrial activities, disrupted calcium homeostasis, and defective mitochondrial function in 3xTg-AD mice 43-47 and APP/PS1,48, both of which are mouse models that produce hyper phosphorylated Tau, supporting the hypothesis that phosphorylated Tau is involved in mitochondrial dysfunction and synaptic damage in AD [26].…”

“…Poly (ethylenimine), poly (alkylcyanoacrylates), poly (amidoamine) dendrimers, poly (-caprolactone), poly (D, L-lactic acid) (PLA), poly (lactic-co-glycolic acid) (PLGA), polyethylene glycol (PEG), and polyesters made of poly (lactic acid) (PLA) are a few examples of synthetic polymer-based NPs. Gold, silica, and carbon are a few examples of inorganic materials for medicinal NPs [20]. Recent research suggests that particular sizes, shapes, and types of sulfur nanoparticles (SNPs) can have the moderating effect against AD pathogenesis, despite the potential implications of certain types of nanoparticles in accelerating AD development [21].…”

"Study of Effects a New Resuspending Solution Which Was Nanotechnologically Upgraded on Lipoperoxidation, Catalase Activity and Red Blood Cell Peroxidation Resistance in Donor Blood Components"

“…Biotechnologies lies primarily in their use as diagnostic tools, drug delivery, and therapy [28][29][30]. Modification of NPs surfaces significantly affects the physical, chemical, and biological nature of entire molecules in biological systems [31].…”

Study of Effects a New Resuspending Solution on Lipoperoxidation, Catalase Activity and Red Blood Cell Peroxidation Resistance in Donor Blood Components

“…It is known that the potential of nanoparticles for medical Biotechnologies lies primarily in their use as diagnostic tools, drug delivery, and therapy [28][29][30]. Modification of NPs surfaces significantly affects the physical, chemical, and biological nature of entire molecules in biological systems [31].…”