Potential Phyto Therapeutic Approaches for the Treatment of Alzheimer’s Disease: An Overview

2020 ◽  
Vol 06 ◽  
Author(s):  
Chetna Kaushik ◽  
Prarthna Yadav

: Alzheimer’s disease is one of the most prevailing age-dependent neurodegenerative disease and the most common cause of dementia. The pharmacological therapies available for the disease provide only symptomatic relief. Plants are being extensively investigated for Alzheimer’s as they are relatively safer and cheaper. This review summarizes recent findings suggesting anti-Alzheimer potential of the plants along with compounds or mechanisms responsible for their efficacy and their therapeutic targets. The findings of recent studies revealed that the plants or the compounds isolated from them exhibit mitigative potential in Alzheimer’s disease by targeting amyloid beta, tau protein, cholinergic pathways via various enzymes like beta secretase, gamma secretase, acetylcholinesterase or receptors involved in these pathways. A number of putative compounds revealed from these studies can be investigated further for the mitigation of Alzheimer’s disease.

2021 ◽  
Vol 11 (9) ◽  
pp. 1211
Author(s):  
Yinyi Xiong ◽  
Chae-Seok Lim

Alzheimer’s disease (AD), the most common neurodegenerative disease, is characterized by progressive cognitive impairment. The deposition of amyloid beta (Aβ) and hyperphosphorylated tau is considered the hallmark of AD pathology. Many therapeutic approaches such as Food and Drug Administration-approved cholinesterase inhibitors and N–methyl–D–aspartate receptor antagonists have been used to intervene in AD pathology. However, current therapies only provide limited symptomatic relief and are ineffective in preventing AD progression. Cannabidiol (CBD), a phytocannabinoid devoid of psychoactive responses, provides neuroprotective effects through both cannabinoid and noncannabinoid receptors. Recent studies using an AD mouse model have suggested that CBD can reverse cognitive deficits along with Aβ-induced neuroinflammatory, oxidative responses, and neuronal death. Furthermore, CBD can reduce the accumulation of Aβ and hyperphosphorylation of tau, suggesting the possibility of delaying AD progression. Particularly, the noncannabinoid receptor, peroxisome proliferator-activated receptor gamma, has been suggested to be involved in multiple functions of CBD. Therefore, understanding the underlying mechanisms of CBD is necessary for intervening in AD pathology in depth and for the translation of preclinical studies into clinical settings. In this review, we summarize recent studies on the effect of CBD in AD and suggest problems to be overcome for the therapeutic use of CBD.


Author(s):  
John-Paul Taylor ◽  
Benjamin R Underwood

Dementia is the fifth leading cause of death worldwide. The most common cause of dementia is Alzheimer’s disease (AD). This fully updated and revised chapter comprehensively reviews the latest evidence on diagnosis, assessment, investigations, clinical features, management, risk factors, prognosis, and future potential treatments for AD. Importantly, the chapter explores newer evidence that has changed the way AD is viewed as regards methods of assessment using various scales to determine diagnosis, as well as current and investigative methods of treating AD. Finally, it looks at the states of disease progression, potential disease-modifying drugs for Alzheimer’s disease, and possible therapeutic approaches to treatment and management.


2012 ◽  
Vol 8 (4S_Part_21) ◽  
pp. S771-S771
Author(s):  
Yoon-Jee Lee ◽  
Jong-Sung Park ◽  
A-Ryeong Gwoan ◽  
Mark Mattson ◽  
Dong-Gyu Jo

2002 ◽  
Vol 38 ◽  
pp. 37-49 ◽  
Author(s):  
Janelle Nunan ◽  
David H Small

The proteolytic processing of the amyloid-beta protein precursor plays a key role in the development of Alzheimer's disease. Cleavage of the amyloid-beta protein precursor may occur via two pathways, both of which involve the action of proteases called secretases. One pathway, involving beta- and gamma-secretase, liberates amyloid-beta protein, a protein associated with the neurodegeneration seen in Alzheimer's disease. The alternative pathway, involving alpha-secretase, precludes amyloid-beta protein formation. In this review, we describe the progress that has been made in identifying the secretases and their potential as therapeutic targets in the treatment or prevention of Alzheimer's disease.


2020 ◽  
Vol 3 (2) ◽  
pp. 216-242 ◽  
Author(s):  
Mayuri Shukla ◽  
Areechun Sotthibundhu ◽  
Piyarat Govitrapong

The revelation of adult brain exhibiting neurogenesis has established that the brain possesses great plasticity and that neurons could be spawned in the neurogenic zones where hippocampal adult neurogenesis attributes to learning and memory processes. With strong implications in brain functional homeostasis, aging and cognition, various aspects of adult neurogenesis reveal exuberant mechanistic associations thereby further aiding in facilitating the therapeutic approaches regarding the development of neurodegenerative processes in Alzheimer’s Disease (AD). Impaired neurogenesis has been significantly evident in AD with compromised hippocampal function and cognitive deficits. Melatonin the pineal indolamine augments neurogenesis and has been linked to AD development as its levels are compromised with disease progression. Here, in this review, we discuss and appraise the mechanisms via which melatonin regulates neurogenesis in pathophysiological conditions which would unravel the molecular basis in such conditions and its role in endogenous brain repair. Also, its components as key regulators of neural stem and progenitor cell proliferation and differentiation in the embryonic and adult brain would aid in accentuating the therapeutic implications of this indoleamine in line of prevention and treatment of AD.   


2020 ◽  
Vol 6 (5) ◽  
pp. 1-7
Author(s):  
Chinonye A Maduagwuna ◽  

Study background: Chronic neuroinflammation is a common emerging hallmark of several neurodegenerative diseases. Alzheimer’s Disease (AD) is the most common cause of dementia among the elderly and is characterized by loss of memory and other cognitive functions.


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