Analyzing the chance of developing dementia among geriatric people: a cross‐sectional pilot study in Bangladesh

Uddin, Md. Sahab; Mamun, Abdullah Al; Takeda, Shinya; Sarwar, Shahid; Begum, Mst. Marium

doi:10.1111/psyg.12368

Cited by 42 publications

(16 citation statements)

References 50 publications

(56 reference statements)

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“…These findings are compatible with a study presenting that lysosomal acidification is malfunctioning in the PS1 knockout principal neurons and fibroblasts in Alzheimer's patients with PS1 mutations (Wolfe et al, 2013). Phase II (Forlenza et al, 2012Nicotinamide Between 1935and 1937 Improvement of autophagy-lysosome processing Phase I (D. Liu, Pitta, et al, 2013 Carbamazepine 1953 Antiepileptic Decrease mTOR activity Xiao, Su, Cao, Sun, and Liang (2010) BECN1 mimetics Autophagy regulator Initiation of autophagy and autophagosome clearance ) Haque, et al, 2016Uddin, Mamun, Takeda, Sarwar, & Begum, 2018). For successful treatment, degradation of toxic molecules is necessary.…”

Section: Ps Dysfunction and Autophagic-lysosomal System In Adsupporting

confidence: 80%

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

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119

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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: Ps Dysfunction and Autophagic-lysosomal System In Adsupporting

confidence: 80%

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

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119

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“…The harmful activities of free radicals and oxidized metabolites in AD include DNA oxidation, lipid peroxidation, and protein oxidation, which ultimately leads to neuronal death [5][6][7][8]. Significant advancement has been achieved to understand AD pathogenesis, since currently available therapeutic methods only deliver moderate relief of cognitive symptoms, such as impairments in perception and memory [9][10][11]. Although, for drug developers, AD has proven to be tremendously challenging, researchers continue to discover better anti-Alzheimer's treatments.…”

Section: Introductionmentioning

confidence: 99%

Molecular Insight into the Therapeutic Promise of Flavonoids against Alzheimer’s Disease

et al. 2020

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Alzheimer’s disease (AD) is one of the utmost chronic neurodegenerative disorders, which is characterized from a neuropathological point of view by the aggregates of amyloid beta (Aβ) peptides that are deposited as senile plaques and tau proteins which form neurofibrillary tangles (NFTs). Even though advancement has been observed in order to understand AD pathogenesis, currently available therapeutic methods can only deliver modest symptomatic relief. Interestingly, naturally occurring dietary flavonoids have gained substantial attention due to their antioxidative, anti-inflammatory, and anti-amyloidogenic properties as alternative candidates for AD therapy. Experimental proof provides support to the idea that some flavonoids might protect AD by interfering with the production and aggregation of Aβ peptides and/or decreasing the aggregation of tau. Flavonoids have the ability to promote clearance of Aβ peptides and inhibit tau phosphorylation by the mTOR/autophagy signaling pathway. Moreover, due to their cholinesterase inhibitory potential, flavonoids can represent promising symptomatic anti-Alzheimer agents. Several processes have been suggested for the aptitude of flavonoids to slow down the advancement or to avert the onset of Alzheimer’s pathogenesis. To enhance cognitive performance and to prevent the onset and progress of AD, the interaction of flavonoids with various signaling pathways is proposed to exert their therapeutic potential. Therefore, this review elaborates on the probable therapeutic approaches of flavonoids aimed at averting or slowing the progression of the AD pathogenesis.

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“…Sequential processing of APP by β- and γ-secretases (Ortega et al, 2013) can cause the formation of neurotoxic Aβ, which can further accumulate as amyloid plaques (Uddin et al, 2019b; Harilal et al, 2019). In contrast, soluble APPα (i.e., non-toxic in nature) is formed due to the α-secretase mediated cleavage of APP (Adeniji et al, 2017).…”

Section: Anti-alzheimer’s In Vitro Studies Of Genisteinmentioning

confidence: 99%

Emerging Signal Regulating Potential of Genistein Against Alzheimer’s Disease: A Promising Molecule of Interest

Uddin

Kabir

2019

Front. Cell Dev. Biol.

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Alzheimer’s disease (AD) is a progressive, irreversible brain disorder characterized by pathological aggregation of the amyloid-β peptide (Aβ) and tau protein; both of these are toxic to neurons. Currently, natural products are regarded as an alternative approach to discover novel multipotent drugs against AD. Dietary soy isoflavone genistein is one of the examples of such agents that occurs naturally and is known to exert a number of beneficial health effects. It has been observed that genistein has the capacity to improve the impairments triggered by Aβ and also it possesses the antioxidant potential to scavenge the AD-mediated generation of free radicals. Furthermore, genistein can interact directly with the targeted signaling proteins and also can stabilize their activity to combat AD. In order to advance the development of AD treatment, a better comprehension of the direct interactions of target proteins and genistein might prove beneficial. Therefore, this article focuses on the therapeutic effects and molecular targets of genistein, which has been found to target directly the Aβ and tau to control the intracellular signaling pathways responsible for neurons death in the AD brain.

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Analyzing the chance of developing dementia among geriatric people: a cross‐sectional pilot study in Bangladesh

Abstract: The outcomes of this study indicated that most of the subjects had MCI or mild dementia and were farmers aged 60-65 years.

Cited by 42 publications

References 50 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

Molecular Insight into the Therapeutic Promise of Flavonoids against Alzheimer’s Disease

Emerging Signal Regulating Potential of Genistein Against Alzheimer’s Disease: A Promising Molecule of Interest

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