Strategies, Development, and Pitfalls of Therapeutic Options for Alzheimer's Disease

Abstract

Therapeutic options for Alzheimer's disease are currently limited to symptomatic treatment that only provides modest and temporary maintenance of cognitive and memory functions, without altering disease progression. Although a variety of therapeutics targeting amyloid production or plaque degradation as well as tau hyperphosphorylation and aggregation have been proposed, examined in pre-clinical models and introduced into clinical trials, many have failed to provide significant therapeutic benefit. Concerns over the adequacy of currently used pre-clinical models, in addition to questions pertaining to the timing of therapeutic administration, vis-à-vis synaptic and neuronal loss have been raised, and are further complicated by the genetic diversity of individual patients. This review will provide a brief overview of Alzheimer's disease pathophysiology and the currently approved therapeutics, while the main section will focus on therapeutics currently evaluated in pre-clinical models and clinical trials.

Nörodejeneratif Hastalıklarda Mezenkimal Kök Hücre Uygulamaları

“…Fakat bu şekilde uygulanan tedaviler sadece belirtilerin ilerlemesini durdurmakta veya kısmi düzelme sağlamaktadır, ancak beyinde oluşan patolojiyi iyileştirmemektedir 69 . Bu nedenle kök hücre uygulamaları hastalığın tedavisi için bir umut ışığı olmuştur.…”

Study of the interaction of Huperzia saururus Lycopodium alkaloids with the acetylcholinesterase enzyme

“…[1] Most of the available treatments have only a palliative effect, providing a temporary retention of cognitive and memory functions, but without altering the disease's progression. [2] In the 70's and in the 80's the basis of the cholinergic hypothesis began to be understood, [3] thereby providing for the first time a rational approach to the treatment of memory loss in AD.…”

Management of Alzheimers Disease: Role of Existing Therapies, Traditional Medicines and New Treatment Targets

“…Neurofibrillary tangles formation takes place as follows [10][11][12] , Tau (τ), a normal constituent of neurons associated with intracellular microtubules gets abnormally phosphorylated and deposited intracellularly as paired helical filaments. After neuronal cell death these filaments aggregate as extracellular neurofibrillary tangles.…”

“…Amyloid plaque (AP) formation takes place as follows [10][11][12] . A type-I transmembrane glycoprotein, amyloid precursor protein (APP) undergoes proteolytic processing through physiologic i.e.…”