scholarly journals A REVIEW ON “NEW TREATMENT STRATEGIES FOR ALZHEIMER’S DISEASE AS NEURODEGENERATIVE DISEASE AND ITS RISK FACTOR CAUSE, SYMPTOMS, AND TREATMENT AT WORLDWIDE”

Author(s):  
Rohit Jaysing Bhor

ABSTRACTAlzheimer’s disease (AD) is a dynamic and irreversible neurodegenerative illness and relates to the most widely recognized reason for dementiaaround the world. AD is a dynamic and lethal cerebrum ailment. Alzheimer’s obliterates mind cells, bringing on memory issue or misfortune and issueswith speculation and conduct sufficiently serious to influence work, long lasting leisure activities or social life. Alzheimer’s illness is quickly becomingworldwide, but there is no cure for it. Now, accessible medications just give symptomatic help and do not mediate in infection prepare adequatelyenough to avert or cure it. Various late studies have reported that working memory does not appear to demonstrate regular age-related deficienciesin solid more established grown-ups when enthusiastic data are included. Indeed, contingent upon the capacity included, patients might demonstratean enthusiastic advantage in their working memory execution. Moreover, this advantage is not generally obviously one-sided (e.g., toward negativeor positive data). We decipher this intricate example of results as an outcome of the cooperation between numerous components including theseriousness of AD, the nature of emotional jolts, and sort of working memory errand. Clinical advantages of the accessible pharmacological treatmentfor AD with antidementia drugs (to be specific cholinesterase inhibitors and Memantine) are obvious. In an unexpected way, learns about the transientcapacity to encode and effectively control enthusiastic data in dementia of Alzheimer’s sort are few and have yielded blended results.Keywords: Alzheimer’s disease, Risk factor for Alzheimer’s disease, Diagnosis, Classification of Anti-Alzheimer’s drug.

2018 ◽  
Vol 39 (4) ◽  
pp. 758-772 ◽  
Author(s):  
Santiago V. Salazar ◽  
Timothy O. Cox ◽  
Suho Lee ◽  
A. Harrison Brody ◽  
Annabel S. Chyung ◽  
...  

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Nicola Mammarella ◽  
Beth Fairfield

A number of recent studies have reported that working memory does not seem to show typical age-related deficits in healthy older adults when emotional information is involved. Differently, studies about the short-term ability to encode and actively manipulate emotional information in dementia of Alzheimer’s type are few and have yielded mixed results. Here, we review behavioural and neuroimaging evidence that points to a complex interaction between emotion modulation and working memory in Alzheimer’s. In fact, depending on the function involved, patients may or may not show an emotional benefit in their working memory performance. In addition, this benefit is not always clearly biased (e.g., towards negative or positive information). We interpret this complex pattern of results as a consequence of the interaction between multiple factors including the severity of Alzheimer’s disease, the nature of affective stimuli, and type of working memory task.


2020 ◽  
Vol 16 (S3) ◽  
Author(s):  
Eva Bagyinszky ◽  
Lindsay A. Farrer ◽  
John Farrell ◽  
Giau Van Vo ◽  
KyuHwan Shim ◽  
...  

Cell Reports ◽  
2020 ◽  
Vol 33 (1) ◽  
pp. 108224
Author(s):  
Priyanka Narayan ◽  
Grzegorz Sienski ◽  
Julia M. Bonner ◽  
Yuan-Ta Lin ◽  
Jinsoo Seo ◽  
...  

Cells ◽  
2019 ◽  
Vol 8 (9) ◽  
pp. 968 ◽  
Author(s):  
Sunitha Kodidela ◽  
Kelli Gerth ◽  
Sanjana Haque ◽  
Yuqing Gong ◽  
Saifudeen Ismael ◽  
...  

The longevity of people with HIV/AIDS has been prolonged with the use of antiretroviral therapy (ART). The age-related complications, especially cognitive deficits, rise as HIV patients live longer. Deposition of beta-amyloid (Aβ), a hallmark of Alzheimer’s disease (AD), has been observed in subjects with HIV-associated neurocognitive disorders (HAND). Various mechanisms such as neuroinflammation induced by HIV proteins (e.g., Tat, gp120, Nef), excitotoxicity, oxidative stress, and the use of ART contribute to the deposition of Aβ, leading to dementia. However, progressive dementia in older subjects with HIV might be due to HAND, AD, or both. Recently, extracellular vesicles (EVs)/exosomes, have gained recognition for their importance in understanding the pathology of both HAND and AD. EVs can serve as a possible link between HIV and AD, due to their ability to package and transport the toxic proteins implicated in both AD and HIV (Aβ/tau and gp120/tat, respectively). Given that Aß is also elevated in neuron-derived exosomes isolated from the plasma of HIV patients, it is reasonable to suggest that neuron-to-neuron exosomal transport of Aβ and tau also contributes to AD-like pathology in HIV-infected subjects. Therefore, exploring exosomal contents is likely to help distinguish HAND from AD. However, future prospective clinical studies need to be conducted to compare the exosomal contents in the plasma of HIV subjects with and without HAND as well as those with and without AD. This would help to find new markers and develop new treatment strategies to treat AD in HIV-positive subjects. This review presents comprehensive literatures on the mechanisms contributing to Aβ deposition in HIV-infected cells, the role of EVs in the propagation of Aβ in AD, the possible role of EVs in HIV-induced AD-like pathology, and finally, possible therapeutic targets or molecules to treat HIV subjects with AD.


2012 ◽  
Vol 510 (1) ◽  
pp. 6-9 ◽  
Author(s):  
Gillian Hamilton ◽  
Kathryn L. Evans ◽  
Donald J. MacIntyre ◽  
Ian J. Deary ◽  
Anna Dominiczak ◽  
...  

2021 ◽  
Author(s):  
Laurie Arnaud ◽  
Philippe Benech ◽  
Louise Greetham ◽  
Delphine Stephan ◽  
Angélique Jimenez ◽  
...  

ABSTRACTThe Apolipoprotein E4 (APOE4) is the major allelic risk factor for late-onset Alzheimer’s disease (AD). APOE4 associates with a pro-inflammatory phenotype increasingly considered as critical in AD initiation and progression. Yet, the mechanisms driving an APOE4-dependent neuroinflammation remain unelucidated. Leveraging patient specific human induced Pluripotent Stem Cells (iPSCs) we demonstrate inflammatory chronicity and hyperactivated responses upon cytokines in human APOE4 astrocytes via a novel mechanism. We uncovered that APOE4 represses Transgelin 3 (TAGLN3), a new interacting partner of IκBα, thus increasing the NF-kB activity. The transcriptional repression of TAGLN3 was shown to result from an APOE4-dependent histone deacetylase (HDAC) activity. The functional relevance of TAGLN3 was demonstrated by the attenuation of APOE4-driven neuroinflammation after TAGLN3 supplementation. Importantly, TAGLN3 downregulation was confirmed in the brain of AD patients. Our findings highlight the APOE4-TAGLN3 axis as a new pathogenic pathway that paves the way for the development of therapeutics to prevent maladaptive inflammatory responses in APOE4 carriers, while placing TAGLN3 downregulation as a potential biomarker of AD.GRAPHICAL ABSTRACT


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. 636-637
Author(s):  
Yaroslav Markov ◽  
Kyra Thrush ◽  
Morgan Levine

Abstract Aging is the major risk factor for Alzheimer’s Disease (AD), and as life expectancy increases, neurodegeneration will continue to afflict an ever-increasing proportion of the population. While numerous theories are attempting to explain the drivers behind AD pathology, what unites them is the observation that AD is reliably associated with a progressive buildup of age-related molecular changes. Because of the varying clinical presentations of AD in patients with similar genetic backgrounds, it has been postulated that epigenetics may be implicated in its etiology. Building on our prior work showing that AD pathology is linked to alterations in age-related DNA CpG methylation (DNAme) across various brain regions, we use state-of-the-art machine learning approaches to identify patterns of molecular damage in postmortem brain samples. We show that alterations in DNAme are associated with accelerated biological aging, AD, and the APOE e4 genotype, which is a major risk factor for AD. We also demonstrate that these associations are present in the PFC but not cerebellum -- in line with the current understanding of AD progression in the brain. Finally, we perform whole-exome sequencing and protein mass spectrometry on the same brain samples to test our hypothesis as to whether AD-associated alterations of DNAme are linked with the accumulation of somatic mutations that affect the structural and binding properties of protein epigenetic regulators.


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