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![The difference between a healthy brain and an AD brain [18].](profile/Benson-Botchway/publication/313846457/figure/fig4/AS:668882582896649@1536485443279/The-difference-between-a-healthy-brain-and-an-AD-brain-18.png)
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![Table 1 . The frequency of the APOE gene [122].](profile/Benson-Botchway/publication/313846457/figure/tbl1/AS:668882582917129@1536485443480/The-frequency-of-the-APOE-gene-122_Q320.jpg)
![Table 2 . Tabulated high risked genes of AD [32, 46-48, 123-128].](profile/Benson-Botchway/publication/313846457/figure/tbl2/AS:668882582896656@1536485443555/Tabulated-high-risked-genes-of-AD-32-46-48-123-128_Q320.jpg)
![Figure 6. The difference between a healthy brain and an AD brain [18].](profile/Benson-Botchway/publication/313846457/figure/fig4/AS:668882582896649@1536485443279/The-difference-between-a-healthy-brain-and-an-AD-brain-18_Q320.jpg)
Alzheimer’s disease (hereafter: AD) is an irreversible, slowly progressive disease of the brain, most often
categorized under the umbrella term ‘neurodegeneration’. It is said to be a progressive disease in a sense that the symptoms associated with AD, the most common one being difficulty in remembering recent events, kick in steadily with the symp...
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Purpose
The purpose of this paper is to examine the moderating role of the demographic variables in emotional intelligence, homesickness and the development of mood swings in university students. Additionally, the paper investigates the relationship among emotional intelligence, homesickness and mood swings in university students.
Design/methodol...
Citations
... Alzheimer's disease (AD) is a progressive neurodegenerative disorder that accounts for the widespread prevalence of dementia in the elderly population [1]. A recent estimate from the World Health Organization indicates that around 55 million individuals have been affected by dementia worldwide. ...
Alzheimer’s disease (AD) is a major form of dementia. Abnormal amyloidogenic event-mediated degeneration of cholinergic neurons in the cognitive centers of the brain has been attributed to neuropathological sequelae and behavioral deficits in AD. Besides, impaired adult neurogenesis in the hippocampus has experimentally been realized as an underlying cause of dementia regardless of neurodegeneration. Therefore, nourishing the neurogenic process in the hippocampus has been considered an effective therapeutic strategy to mitigate memory loss. In the physiological state, the Wnt pathway has been identified as a potent mitogenic generator in the hippocampal stem cell niche. However, downstream components of Wnt signaling have been noticed to be downregulated in AD brains. Resveratrol (RSV) is a potent Sirtuin1 (SIRT1) enhancer that facilitates neuroprotection and promotes neurogenesis in the hippocampus of the adult brain. While SIRT1 is an important positive regulator of Wnt signaling, ample reports indicate that RSV treatment strongly mediates the fate determination of stem cells through Wnt signaling. However, the possible therapeutic roles of RSV-mediated SIRT1 enhancement on the regulation of hippocampal neurogenesis and reversal of memory loss through the Wnt signaling pathway have not been addressed yet. Taken together, this review describes RSV-mediated effects on the regulation of hippocampal neurogenesis via the activation of SIRT1 in synergy with the Wnt signaling. Further, the article emphasizes a hypothesis that RSV treatment can provoke the activation of quiescent neural stem cells and prime their neurogenic capacity in the hippocampus via Wnt signaling in AD.
... It maintains cell wall integrity and acts as a building block for many hormones (such as testosterone, cortisol, and aldosterone). Lipoproteins comprise apolipoprotein and lipids and transport cholesterol through the bloodstream [1,42]. Apolipoproteins include apolipoprotein A-1 (APOA-I), apolipoprotein B-48 (APOB-48), apolipoprotein C-II (APOC-II), and apolipoprotein E (APOE). ...
... For instance, APOC-II functions in energy delivery and storage through its hydrolyzation of chylomicrons and very-low-density lipoprotein (VLDL) [43]. We have previously reported the multiple polymorphic alleles of APOE and their frequency in humans [1]. APOE-ε4, in particular, has been associated with late-onset AD [44][45][46]. ...
Alzheimer's disease (AD) is a current public health challenge and will remain until the development of an effective intervention. However, developing an effective treatment for the disease requires a thorough understanding of its etiology, which is currently lacking. Although several studies have shown the association between oxidative damage and AD, only a few have clarified the specific mechanisms involved. Herein, we reviewed recent preclinical and clinical studies that indicated the significance of oxidative damage in AD, as well as potential antioxidants. Although several factors regulate oxidative stress in AD, we centered our investigation on apolipoprotein E and the gut microbiome. Apolipoprotein E, particularly apolipoprotein E-ε4, can impair the structural facets of the mitochondria. This, in turn, can minimize the mitochondrial functionality and result in the progressive build-up of free radicals, eventually leading to oxidative stress. Similarly, the gut microbiome can influence oxidative stress to a significant degree via its metabolite, trimethylamine N-oxide. Given the various roles of these two factors in modulating oxidative stress, we also discuss the possible relationship between them and provide future research directions.
... Oxidative stress occurs in several human chronic diseases but has been strongly implicated in aging and neurodegenerative diseases (Salganik, 2001;Fridovich, 1999). Indeed, studies have demonstrated that oxidative stress can lead to the accumulation and aggregation of Aβ in AD patients brains (Botchway Bo, 2017). Studies from postmortem brains revealed age-dependent increase of oxidative damages (oxidized proteins, lipids, ...
Alzheimer′s disease (AD) is by far the most prevalent neurodegenerative disease of aging and is a major burden for patients, caregivers, and the overall health care system. The complexity of AD pathophysiology and the lack of deep understanding of disease mechanisms impeded the development of AD therapy. Currently approved treatments for AD only modestly improve cognitive function but do not modify disease course. The lack of pharmacological approaches has led to the consideration of alternative strategies to prevent or to slow down the progression of AD. There has been a growing interest in the scientific community regarding the impact of diet and nutrition on AD. Grape derived nutraceuticals and phytochemical compounds have demonstrated anti-amyloidogenic, antioxidative, anti-inflammatory and neurotrophic properties and present as potential novel strategies for AD treatment. In this review, we summarize promising grape derived polyphenols that have been shown to modulate AD pathophysiology including amyloid plaques and neurofibrillary tangles formation, AD-induced oxidative stress, neuroinflammation and synaptic dysfunction.
... Two primary causes responsible for the loss of Ach are either an accelerated degradation rate (due to enhanced acetylcholinesterase levels) or Ach or cholinergic neuron destruction, which results in the loss of cholinergic stimulation, which is essential for behavioral functions [9,10]. Therefore, acetylcholinesterase inhibitors are conventionally recognized as first-line drugs in AD treatment, mainly comprising rivastigmine, galantamine and donepezil, which are commonly employed in mild AD cases [11]. However, after the first 3 months of observed improvement in the condition of AD patients, the action of these compounds is reduced due to the development of tolerance [2]. ...
One of the most commonly occurring neurodegenerative disorders, Alzheimer's Disease 15 (AD), encompasses loss of cognitive and memory potential, impaired learning, dementia and 16 behavioral defects, which has prevalent since the 1900s. The accelerating occurrence of AD is 17 expected to reach 65.7 million by 2030. The disease results in neural atrophy and disrupted inter 18 neuronal connections. Amongst multiple AD pathogenesis hypothesis, the amyloid beta (Aβ) 19 cascade is the most relevant and accepted form of hypothesis, which suggests that Aβ monomers 20 are formed as a result of cleavage of amyloid precursor protein (APP), followed by the conversion 21 of these monomers to toxic oligomers, which in turn develop β-sheets, fibrils and plaques. The 22 review targets the events in the amyloid hypothesis and elaborates suitable therapeutic agents, that 23 function by hindering the steps of plaque formation and abbreviating Aβ levels in the brain. The 24 authors discuss treatment possibilities, including, inhibition of β-and γ-secretase mediated 25 enzymatic cleavage of APP, immune response generating active immunotherapy and passive 26 immunotherapeutic approaches targeting monoclonal antibodies towards Aβ aggregates, removal 27 of amyloid aggregates by activation of enzymatic pathways or regulation of Aβ circulation, 28 glucagon-like peptide-1 (GLP-1) mediated curbed accumulation and neurotoxic potential of Aβ 29 aggregates, bapineuzumab mediated vascular permeability alterations, statins mediated Aβ peptide 30 degradation, potential role of ibuprofen and significance of natural drugs and dyes in hindering the 31 amyloid cascade events. Thus, the authors aim to highlight the treatment perspective, targeting 32 amyloid hypothesis, simultaneously emphasizing on the need to conduct further investigations, in 33 order to provide an opportunity to the neurologists to develop novel and reliable treatment 34 therapies in retardation of AD progression. 35
... Alzheimer's disease (AD) is one of many neurodegenerative diseases, including Parkinson's disease, Huntington's disease, and normal pressure hydrocephalus [1]. AD continues to pose a great challenge to the aging community, especially those in developed countries. ...
... In our previous published report, we explicated the history of the disease as well as ongoing developments regarding treatment methods along with other currently researched therapeutics. slow down the inevitable [1]. A few months back, Solanezumab, a monoclonal antibody that showed stupendous potentiality as being future therapeutic for mild AD, failed in its final clinical trial, Expedition 3. Though the drug, to some extent, might have inhibited soluble amyloid- (A), the cognitive decline associated with the disease was not statistically conspicuous when the treatment group was compared to the placebo group [2]. ...
... The connection between nutrition and AD has been discussed in several published studies. In some quarters, curcumin, vitamins, and Mediterranean diet have been postulated to possibly have a preventative role in AD [1,[7][8][9]. As such, this review report was centered on these three nutritional components. ...
Since its discovery some hundred years ago, Alzheimer’s disease (AD), a neurodegenerative disease and an eminent cause of most dementia, continues to pose problems for affected families and society, especially in developed countries. With the approved medications by the Food and Drugs Administration in the United States, effectual treatment of AD apropos to the complete eradication of the disease continues to be elusive due to complexities relating to the pathophysiology of the disease. Nutrition has and continues to play a salient role in the survival of living organisms with no exception for human beings. Herein, we report the connection between nutrition and AD with particular attention to vitamins, curcumin, and the Mediterranean diet.
... DNA methylation as well as histone modification has been associated to depression [16,17]. Epigenetics generally is the change in role of gene without making adjustments to the DNA sequence [18]. In a study carried out using 9-11 week old C57BL/65 male mice, researchers found histone H3 acetylation and HDAC 2, a class-1 type of histone deacetylase, to be increased and decreased respectively in the nucleus accumbens of both depressed mice and autopsied depressed humans. ...
Background: Depression is a debilitating disease that is affecting a growing number of patients, both physically and mentally. In addition to mood changes, depression results in cognitive impairment. Although depression studies have been going on for decades, the underlying mechanism still remains unclear. MicroRNAs (miRNAs), a type of small non-coding RNAs, predominantly control the expression of their target mRNAs to exert their functions. Some evidences have revealed the importance of miRNAs in the mechanism of depression,however, these studies are still in their infancy. Alterations in brain regions, synaptic plasticity, hypothalamic-pituitary-adrenal (HPA) axis, changes in the levels of serotonin and glucocorticoids, together with stress response have been proven to be involved in depression. These alterations can influence cognition, learning and memory, with recent evidences demonstrating the involvement of miRNAs in several aspects of stress response, neural plasticity and neurogenesis as well as pathogenesis of depression.
Objective: In light of these theories of depression, this review was aimed at elucidating the role of miRNAs in the underlying mechanisms of depression resulting in cognitive, learning and memory impairments.
Method/Results: Both PubMed and Scopus databases were employed in scouring for research reports pertaining to this area of study. A total of 180 articles were obtained from these two databases.
Conclusion: With the probing of classical theories of depression as well as the connection between miRNAs and depression, more studies, nevertheless, are needed to ascertain the full mechanism of depression along with its resultant cognitive, learning and memory impediments.
During the geriatric phase of life, human beings are more susceptible to severe brain diseases. They usually forget things and hardly memorize matters, which is the real cause of Alzheimer. There are limitations in preventing such diseases; therefore, the scientific community focuses on the safety strategies for the same. Elaborative preclinical and clinical studies and an extensive study on the cognitive decline at an early stage played a significant role in managing the disease. This review deals with recent advancements in specified brain foods and their effect on cognitive aging. Furthermore, several key points were also mentioned related to the pathophysiology of the disease affecting brain functions. This manuscript also elaborates mechanisms of some recent phytomedicines and their role in treatment, covering specific research gaps, suggesting a new domain of research portfolios that inform dietary recommendations to prevent disease severity.KeywordsBrain foodsCognitive declineBrain functionsPhytomedicine
