Drugs and Drug Delivery Systems Targeting Amyloid-\b{eta} in Alzheimers Disease

TL;DR

This paper reviews drugs and delivery systems targeting amyloid-beta to treat Alzheimer's disease, emphasizing the challenge of crossing the blood-brain barrier and the need for innovative delivery methods.

Contribution

It provides a comprehensive overview of anti-amyloid-beta drugs and discusses the importance of advanced delivery systems to overcome the blood-brain barrier in Alzheimer's treatment.

Findings

Many anti-Aβ drugs show success in vitro and in animal models.

Delivery systems are crucial for effective drug transport across the blood-brain barrier.

Targeting Aβ aggregation could facilitate natural clearance in Alzheimer's therapy.

Abstract

Alzheimer's disease (AD) is a devastating neurodegenerative disorder with no cure and limited treatment solutions that are unable to target any of the suspected causes. Increasing evidence suggests that one of the causes of neurodegeneration is the overproduction of amyloid beta (A\b{eta}) and the inability of A\b{eta} peptides to be cleared from the brain, resulting in self-aggregation to form toxic oligomers, fibrils and plaques. One of the potential treatment options is to target A\b{eta} and prevent self-aggregation to allow for a natural clearing of the brain. In this paper, we review the drugs and drug delivery systems that target A\b{eta} in relation to Alzheimer's disease. Many attempts have been made to use anti-A\b{eta} targeting molecules capable of targeting A\b{eta} (with much success in vitro and in vivo animal models), but the major obstacle to this technique is the challenge posed by the blood brain barrier (BBB). This highly selective barrier protects the brain from toxic molecules and pathogens and prevents the delivery of most drugs. Therefore novel A\b{eta} aggregation inhibitor drugs will require well thought-out drug delivery systems to deliver sufficient concentrations to the brain.