Abstract
Alzheimer’s disease (AD) is a serious health concern, affecting millions of people globally, which leads to cognitive impairment, dementia, and inevitable death. There is still no medically accepted treatment for AD. Developing therapeutic treatments for AD is an overwhelming challenge in the medicinal field, as the exact mechanics underlying its devastating symptoms is still not completely understood. Rather than the unknown mechanism of the disease, one of the limiting factors in developing new drugs for AD is the blood–brain barrier (BBB). A combination of nanotechnology with fluorinated molecules is proposed as a promising therapeutic treatment to meet the desired pharmacokinetic/physiochemical properties for crossing the BBB passage. This paper reviews the research conducted on fluorine-containing compounds and fluorinated nanoparticles (NPs) that have been designed and tested for the inhibition of amyloid-beta (Aβ) peptide aggregation. Additionally, this study summarizes fluorinated molecules and NPs as promising agents and further future work is encouraged to be effective for the treatment of AD.
Highlights
Alzheimer’s disease (AD) is a progressive and irreversible neurodegenerative disease [1] and is responsible for about 70% of all late-onset dementia cases [2]
Deaths reported from heart diseases and various types of cancer have decreased since 2000, whereas deaths from AD have increased to 145% [3]
In the last two decades, the fluorine-containing compounds have attracted a great deal of academic and industrial interest owing to the overall remarkable properties like high metabolic stability, distribution, and excretion properties etc
Summary
Alzheimer’s disease (AD) is a progressive and irreversible neurodegenerative disease [1] and is responsible for about 70% of all late-onset dementia cases [2]. Deaths reported from heart diseases and various types of cancer have decreased since 2000, whereas deaths from AD have increased to 145% [3] This reveals the lack of therapies in the field of AD. Current therapeutics available for the treatment for AD only relieve symptoms, cannot terminate/reverse the aggregation of amyloid deposits in the brain. This leads to the serious concern and urgent need for disease modifying treatments that can prevent, delay, and slow down the progression by targeting one of the most evident key pathophysiology mechanisms that cause AD [14,15]. The current study reveals the powerful role of fluorine for the inhibition of anti-amyloid aggregation and suggests a new therapeutic approach of fluorine in combination with nanotechnology. Papers written in English were considered with unlimited publication date
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