Neuroprotective Activity of Asparagus racemosus Linn. Against Ethanol- Induced Cognitive Impairment and Oxidative Stress in Rats Brain: Auspicious for Controlling the Risk of Alzheimer’s Disease

Asaduzzaman, Md.

doi:10.4172/2161-0460.1000245

Cited by 34 publications

(26 citation statements)

References 49 publications

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“…Thus tau regulates the vesicle passage in neurons. When tau is abnormally hyperphosphorylated by tau kinases, it forms NFTs (Uddin, Mamun, Iqbal et al, ). The maturation of autolysosome and their retrograde passage are hindered in AD that causes an enormous deposit of autophagic vacuoles (Brion, ).…”

Section: Introductionmentioning

confidence: 99%

Autophagic dysfunction in Alzheimer’s disease: Cellular and molecular mechanistic approaches to halt Alzheimer’s pathogenesis

Uddin

Mamun

Labu

et al. 2018

Journal Cellular Physiology

120

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Autophagy is a preserved cytoplasmic self‐degradation process and endorses recycling of intracellular constituents into bioenergetics for the controlling of cellular homeostasis. Functional autophagy process is essential in eliminating cytoplasmic waste components and helps in the recycling of some of its constituents. Studies have revealed that neurodegenerative disorders may be caused by mutations in autophagy‐related genes and alterations of autophagic flux. Alzheimer’s disease (AD) is an irrevocable deleterious neurodegenerative disorder characterized by the formation of senile plaques and neurofibrillary tangles (NFTs) in the hippocampus and cortex. In the central nervous system of healthy people, there is no accretion of amyloid β (Aβ) peptides due to the balance between generation and degradation of Aβ. However, for AD patients, the generation of Aβ peptides is higher than lysis that causes accretion of Aβ. Likewise, the maturation of autophagolysosomes and inhibition of their retrograde transport creates favorable conditions for Aβ accumulation. Furthermore, increasing mammalian target of rapamycin (mTOR) signaling raises tau levels as well as phosphorylation. Alteration of mTOR activity occurs in the early stage of AD. In addition, copious evidence links autophagic/lysosomal dysfunction in AD. Compromised mitophagy is also accountable for dysfunctional mitochondria that raises Alzheimer’s pathology. Therefore, autophagic dysfunction might lead to the deposit of atypical proteins in the AD brain and manipulation of autophagy could be considered as an emerging therapeutic target. This review highlights the critical linkage of autophagy in the pathogenesis of AD, and avows a new insight to search for therapeutic target for blocking Alzheimer’s pathogenesis.

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Section: Introductionmentioning

confidence: 99%

Autophagic dysfunction in Alzheimer’s disease: Cellular and molecular mechanistic approaches to halt Alzheimer’s pathogenesis

Uddin

Mamun

Labu

et al. 2018

Journal Cellular Physiology

120

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“…AD is not a typical part of normal aging. The supreme well-known threatening factor is aging, and the mainstreams of people with AD are 65 years and older [2]. In fact, AD is not considered as a disease of adulthood.…”

Section: Introductionmentioning

confidence: 99%

Introductory Chapter: Alzheimer’s Disease—The Most Common Cause of Dementia

Ashraf¹

2019

Advances in Dementia Research

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“…The powdered dried roots of A. racemosus have traditionally been used in Ayurveda for galactogogue (Sharma et al, 1996). Several papers have reported its roots to have many medicinal activities including anti-oxidant (Kamat et al, 2000;Wiboonpun et al, 2004;Uddin et al, 2016) antifungal (Onlom et al, 2014) anti-cancer ( Ji et al, 2012) and anti-epileptogenic (Pahwa and Goel 2016). In vivo, A. racemosus extracts showed hepatoprotective and gastroprotective activity against various aliments as well as reduced lipid peroxidation ( Jayashree et al, 2015) although the molecular species and the mechanisms involved are still yet, unclear.…”

Section: Introductionmentioning

confidence: 99%

“…Malondialdehyde (MDA), the final oxidation product lipid peroxidation, is more prominent in tumours than in normal tissues (Sekine et al, 1997). While many reports have shown that A. racemosus root extracts have "antioxidant" activity (Kamat et al, 2000;Wiboonpun et al, 2004;Uddin et al, 2016), there are no reports indicating that its saponins may prevent lipid peroxidation.…”

Section: Introductionmentioning

confidence: 99%

Immunoaffinity Knockout of Saponin Glycosides from Asparagus racemosus to Assess Anti‐lipid Peroxidation

Onlom

Phrompittayarat

Putalun

et al. 2017

Phytochemical Analysis

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Neuroprotective Activity of Asparagus racemosus Linn. Against Ethanol- Induced Cognitive Impairment and Oxidative Stress in Rats Brain: Auspicious for Controlling the Risk of Alzheimer’s Disease

Cited by 34 publications

References 49 publications

Autophagic dysfunction in Alzheimer’s disease: Cellular and molecular mechanistic approaches to halt Alzheimer’s pathogenesis

Autophagic dysfunction in Alzheimer’s disease: Cellular and molecular mechanistic approaches to halt Alzheimer’s pathogenesis

Introductory Chapter: Alzheimer’s Disease—The Most Common Cause of Dementia

Immunoaffinity Knockout of Saponin Glycosides from Asparagus racemosus to Assess Anti‐lipid Peroxidation

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