Alzheimer’s Disease: Perspective on Therapeutic Options and Recent Hallmarks in Clinical Research

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative, a primarily concerned and leading cause of mortality worldwide which has no cure so far, of the world. The disease progresses from memory loss to cognitive decline gradually. The severity of Alzheimer's grows up from mild, moderate to severe. Hallmarks of the research of AD reported, are the identification of amyloid-beta (Aβ) plaques and tau protein tangles between and within the neuronal cells, oxidative stress, low acetylcholine, and most importantly the genetic connection. Diagnosis of this condition is not so simple since there is no single test that identifies Alzheimer's as early as possible. The therapies for the disease just provide symptomatic relief but not cure. The present review emphasizes the disease burden in the world, neurobiological aspects, and its management through conventional drug therapies along with novel research on therapeutic strategies, new drugs which showed excellent results that are to be approved and were approved, including investigations on plant medicine.

A New Perspective for the Treatment of Alzheimer’s Disease: Exosome-Like Liposomes to Deliver Natural Compounds and RNA Therapies

“…The amyloidogenic pathway includes the combined action of βand γsecretases, which generate Aβ peptides with different C-terminal residues (Aβ 40 and Aβ 42 ) [15,27]. The deposition and accumulation of these Aβ polypeptides lead to the formation of amyloid plaques in the brain, resulting in neuroinflammation and synaptic dysfunction [30][31][32]. NFTs are a consequence of the deposition of the abnormally phosphorylated Tau protein, leading to its aggregation [16].…”

A New Perspective for the Treatment of Alzheimer’s Disease: Exosome-like Liposomes to Deliver Natural Compounds and RNA Therapies

“…The amyloidogenic pathway includes the combined action of β- and γ- secretases, which generate Aβ peptides with different C-terminal residues (Aβ 40 and Aβ 42 ) [ 15 , 27 ]. The deposition and accumulation of these Aβ polypeptides lead to the formation of amyloid plaques in the brain, resulting in neuroinflammation and synaptic dysfunction [ 30 , 31 , 32 ]. NFTs are a consequence of the deposition of the abnormally phosphorylated Tau protein, leading to its aggregation [ 16 ].…”