Future Treatment of Alzheimer Disease

Abstract

Alzheimer's disease is an age-related progressive neurodegenerative disorder. The two major neuropathologic hallmarks of Alzheimer's disease (AD) are extracellular Amyloid beta (Aβ) plaques and intracellular neurofibrillary tangles (NFTs). A number of additional pathogenic mechanisms, possibly overlapping with Aβ plaques and NFTs formation, have been described, including inflammation, oxidative damage, iron dysregulation, cholesterol metabolism. To date, only symptomatic treatments exist for this disease, all trying to counterbalance the neurotransmitter disturbance. To block the progression of the disease they have to interfere with the pathogenic steps responsible for the clinical symptoms, including the deposition of extracellular amyloid β plaques and intracellular neurofibrillary tangle formation, inflammation and stem cell. In this review, we discuss new potential disease-modifying therapies for AD that are currently being studied in phase I-III trials.

Identification of potential neuroprotective compound from Ganoderma lucidum extract targeting microtubule affinity regulation kinase 4 involved in Alzheimer's disease through molecular dynamics simulation and MMGBSA

“…It describes the absorption, distribution, drug metabolism, and excretion of a substance or medication 19,20 . Solubility and permeability are critical characteristics that influence the oral absorption rate 21,22 . As soon as the medication is dissolved, it circulates throughout the body and is distributed throughout different systems.…”

“… 19 , 20 Solubility and permeability are critical characteristics that influence the oral absorption rate. 21 , 22 As soon as the medication is dissolved, it circulates throughout the body and is distributed throughout different systems. Drug distribution into tissues and organs is governed by pharmacokinetic characteristics, such as plasma protein binding, lipophilicity, and phospholipids, three essential variables to consider.…”

Progress in the development of naturally derived active metabolites‐based drugs: Potential therapeutics for Alzheimer's disease

“…This causes malfunction within the communication in between the neuronal cells, leading to apoptosis 17,18 . Recently, most of the articles documented that only tau protein could not initiate AD pathogenesis and both Aβ and tau protein abnormalities are responsible to offer a precise disease diagnosis 19–23 . Numerous reports have investigated the interaction as well as progression of both these pathophysiologies, which provided additional evidence that amyloid pathology develop several years prior to the exhibiting clinical symptoms, whereas tau pathophysiology develop afterward 24,25 …”

Potential of Medicinal Plants as Neuroprotective and Therapeutic Properties Against Amyloid-β-Related Toxicity, and Glutamate-Induced Excitotoxicity in Human Neural Cells

“…The therapeutic approach in the management and treatment of AD is to decrease amyloid levels, prevent amyloid aggregation/toxicity, as well as tau phosphorylation/aggregation [ 40 ]. There are four types of treatments for AD that have effectively progressed to advanced phases in clinical trials, namely (1) immunotherapies, (2) secretase inhibitors, (3) selective Aβ 42 -lowering agents (SALAs), and (4) anti-Aβ aggregation agents [ 41 ].…”