scholarly journals A Global Review on Alzheimer’s Disease

2021 ◽  
Vol 68 (1) ◽  
Author(s):  
Natarajan. P ◽  
Mumthaj. P ◽  
Vijay. J ◽  
Gokul. V
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cholinesterase Inhibitors ◽  
Genetic Factors ◽  
Environmental Changes ◽  
Late Onset ◽  
Memory Loss ◽  
Review Article ◽  
Acetyl Cholinesterase ◽  
Alois Alzheimer

Alzheimer’s disease (AD) is an inevitable neurological disorder in which the death of brain cells causes memory loss and cognitive decline and ultimate dementia. It’s the foremost common cause of dementia in people of 65 years and older. It was first described by a neurologist Alois Alzheimer in 1906. This review article gives an account on the various symptoms from pre-dementia to severe Alzheimer’s dementia. The Alzheimer’s disease is caused by the pathogenesis by accumulation of toxic amyloid-? plaques (A?) and Hyper phosphorylated tau (p-tau). The greatest risk factors for late onset Alzheimer’s are age, genetics, family history and non-genetic factors (heart health, life style modifications, and environmental changes). The diagnosis of AD advances in genetics, the event of biomarkers of neuro degeneration and neuroimaging discovery utilizes the method to detect AD. The medication use to treat AD is acetyl cholinesterase inhibitors and N-methyl D aspartate antagonists and various drugs are under clinical trials.

scholarly journals Autophagy and mitophagy biomarkers are reduced in sera of patients with Alzheimer’s disease and mild cognitive impairment

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Massimiliano Castellazzi ◽  
Simone Patergnani ◽  
Mariapina Donadio ◽  
Carlotta Giorgi ◽  
Massimo Bonora ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Late Onset ◽  
Memory Loss ◽  
Serum Levels ◽  
Enzyme Linked Immunosorbent Assay ◽  
Serum Samples ◽  
Cellular Processes

AbstractDementia is a neurocognitive disorder characterized by a progressive memory loss and impairment in cognitive and functional abilities. Autophagy and mitophagy are two important cellular processes by which the damaged intracellular components are degraded by lysosomes. To investigate the contribution of autophagy and mitophagy in degenerative diseases, we investigated the serum levels of specific autophagic markers (ATG5 protein) and mitophagic markers (Parkin protein) in a population of older patients by enzyme-linked immunosorbent assay. Two hundred elderly (≥65 years) outpatients were included in the study: 40 (20 F and 20 M) with mild-moderate late onset Alzheimer’s disease (AD); 40 (20 F and 20 M) affected by vascular dementia (VAD); 40 with mild cognitive impairment (MCI); 40 (20 F and 20 M) with “mixed” dementia (MD); 40 subjects without signs of cognitive impairment were included as sex-matched controls. Our data indicated that, in serum samples, ATG5 and Parkin were both elevated in controls, and that VAD compared with AD, MCI and MD (all p < 0.01). Patients affected by AD, MD, and MCI showed significantly reduced circulating levels of both ATG5 and Parkin compared to healthy controls and VAD individuals, reflecting a significant down-regulation of autophagy and mitophagy pathways in these groups of patients. The measurement of serum levels of ATG5 and Parkin may represent an easily accessible diagnostic tool for the early monitoring of patients with cognitive decline.

scholarly journals East Asian-specific novel loci associated with late-onset Alzheimer’s disease: the GARD cohort Genome-wide study

2020 ◽  
Author(s):  
Sarang Kang ◽  
Tamil Iniyan Gunasekaran ◽  
Kyu Yeong Choi ◽  
Jang Jae Lee ◽  
Sungho Won ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Large Scale ◽  
Genetic Factors ◽  
Late Onset ◽  
East Asian ◽  
Genetic Heritability ◽  
Genome Wide ◽  
Japanese Sample ◽  
Genomic Studies

ABSTRACTThe high genetic heritability of Alzheimer’s disease has contributed to the multi-directional and large-scale genomic studies to discover genetic factors, and so far many massive studies have been reported. However, the majority of genetic factors have been identified through European races, and relatively few studies using East Asians to discover genetic factors. In this study, East Asian specific loci is first reported through GWAS using GARD cohorts, which have been intensively recruited and managed by a single institution. ApoE-stratified GWAS with the AD cases and matched controls (n=2,291) in the Korean cohort and validation analysis using a Japanese sample (n=1,956) replicated six previously reported loci (genes) including ApoE and suggested two novel susceptible loci in LRIG1 and CACNA1A gene. This study demonstrates that discovery of AD-associated variants can be accomplished in ethnic groups of a more homogeneous genetic background using samples comprising fewer subjects.

A Systematic Review on Donepezil-based Derivatives as Potential Cholinesterase Inhibitors for Alzheimer’s Disease

2019 ◽  
Vol 26 (30) ◽  
pp. 5625-5648 ◽  
Author(s):  
Jan Korabecny ◽  
Katarina Spilovska ◽  
Eva Mezeiova ◽  
Ondrej Benek ◽  
Radomir Juza ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cholinesterase Inhibitors ◽  
Neurodegenerative Disorder ◽  
Memory Loss ◽  
Nmda Receptor Antagonist ◽  
Amyloid Burden ◽  
Ache Inhibitors ◽  
Intellectual Capacity ◽  
Β Amyloid

: Alzheimer’s Disease (AD) is a multifactorial progressive neurodegenerative disorder characterized by memory loss, disorientation, and gradual deterioration of intellectual capacity. Its etiology has not been elucidated yet. To date, only one therapeutic approach has been approved for the treatment of AD. The pharmacotherapy of AD has relied on noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist - memantine, and acetylcholinesterase (AChE) inhibitors (AChEIs) - tacrine, donepezil, rivastigmine and galantamine. Donepezil was able to ameliorate the symptoms related to AD mainly via AChE, but also through reduction of β-amyloid burden. This review presents the overview of donepezilrelated compounds as potential anti-AD drugs developed on the basis of cholinergic hypothesis to act as solely AChE and butyrylcholinesterase (BChE) inhibitors.

Strategic approaches to target the enzymes using natural compounds for the management of Alzheimer’s disease: A review

2021 ◽  
Vol 20 ◽  
Author(s):  
Syed Sayeed Ahmad ◽  
Kaiser Younis ◽  
Jeandet Philippe ◽  
Michael Aschner ◽  
Haroon Khan
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Molecular Mechanisms ◽  
Genetic Factors ◽  
Cholesterol Metabolism ◽  
Memory Loss ◽  
Amyloid Plaques ◽  
Natural Compounds ◽  
Neurological Deficits ◽  
Hyperphosphorylated Tau Protein

: Alzheimer's disease (AD) is a chronic neurodegenerative disease. It is clinically characterized by memory loss and intellectual decrease, among other neurological deficits. The etiology of AD is not completely understood but includes amyloid plaques and intracellular helical filaments as well as neurofibrillary tangles with hyperphosphorylated tau protein. AD is also associated with alterations in amyloid processing genes, such as PSEN1 or PSEN2 and APP. The modulation immune system, cholesterol metabolism, and synaptic vesicle endocytosis have all been shown to remediate AD. In this review, enzymes such as AChE, BuChE, β-secretase, γ-secretase, MAO, and RAGE are discussed as potential targets for AD treatment. The aim of this review was to addresses the molecular mechanisms as well as various genetic factors in AD etiology. The use of natural compounds against these targets might be beneficial for the management of AD.

scholarly journals Epigenetic Factors in Late-Onset Alzheimer’s Disease: MTHFR and CTH Gene Polymorphisms, Metabolic Transsulfuration and Methylation Pathways, and B Vitamins

2019 ◽  
Vol 20 (2) ◽  
pp. 319 ◽  
Author(s):  
Gustavo Román ◽  
Oscar Mancera-Páez ◽  
Camilo Bernal
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Methylenetetrahydrofolate Reductase ◽  
Late Onset ◽  
Memory Loss ◽  
B Vitamins ◽  
Common Mutation ◽  
Epigenetic Factors ◽  
Vitamin B9 ◽  
Transsulfuration Pathway

DNA methylation and other epigenetic factors are important in the pathogenesis of late-onset Alzheimer’s disease (LOAD). Methylenetetrahydrofolate reductase (MTHFR) gene mutations occur in most elderly patients with memory loss. MTHFR is critical for production of S-adenosyl-l-methionine (SAM), the principal methyl donor. A common mutation (1364T/T) of the cystathionine-γ-lyase (CTH) gene affects the enzyme that converts cystathionine to cysteine in the transsulfuration pathway causing plasma elevation of total homocysteine (tHcy) or hyperhomocysteinemia—a strong and independent risk factor for cognitive loss and AD. Other causes of hyperhomocysteinemia include aging, nutritional factors, and deficiencies of B vitamins. We emphasize the importance of supplementing vitamin B12 (methylcobalamin), vitamin B9 (folic acid), vitamin B6 (pyridoxine), and SAM to patients in early stages of LOAD.

STUDYING THE ROLE OF ApoE IN ALZHEIMER'S DISEASE PATHOGENESIS USING A SYSTEMS BIOLOGY MODEL

2013 ◽  
Vol 11 (05) ◽  
pp. 1342003 ◽  
Author(s):  
CHRISTINA ROSE KYRTSOS ◽  
JOHN S. BARAS
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Systems Biology ◽  
Systems Approach ◽  
Late Onset ◽  
Memory Loss ◽  
Short Term ◽  
Disease Pathogenesis ◽  
Amyloid Aβ ◽  
Initiating Factors

Alzheimer's disease (AD) is the most common form of dementia. Even with its well-known symptoms of memory loss and well-characterized pathology of beta amyloid (Aβ) plaques and neurofibrillary tangles, the disease pathogenesis and initiating factors are still not well understood. To tackle this problem, a systems biology model has been developed and used to study the varying effects of variations in the ApoE allele present, as well as the effects of short term and periodic inflammation at low to moderate levels. Simulations showed a late onset peak of Aβ in the ApoE4 case that lead to localized neuron loss which could be ameliorated in part by application of short-term pro-inflammatory mediators. The model that has been developed herein represents one of the first attempts to model AD from a systems approach to study physiologically relevant parameters that may prove useful to physicians in the future.

scholarly journals Dedifferentiation orchestrated through remodeling of the chromatin landscape defines PSEN1 mutation-induced Alzheimer’s Disease

2019 ◽  
Author(s):  
Andrew B. Caldwell ◽  
Qing Liu ◽  
Gary P. Schroth ◽  
Rudolph E. Tanzi ◽  
Douglas R. Galasko ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neurodegenerative Disorder ◽  
Late Onset ◽  
Disease Model ◽  
Memory Loss ◽  
Amyloid Β ◽  
Chromatin Accessibility ◽  
Experimental Models ◽  
Patient Specific

AbstractEarly-Onset Familial Alzheimer’s Disease (EOFAD) is a dominantly inherited neurodegenerative disorder elicited by mutations in the PSEN1, PSEN2, and APP genes1. Hallmark pathological changes and symptoms observed, namely the accumulation of misfolded Amyloid-β (Aβ) in plaques and Tau aggregates in neurofibrillary tangles associated with memory loss and cognitive decline, are understood to be temporally accelerated manifestations of the more common sporadic Late-Onset Alzheimer’s Disease. The complete penetrance of EOFAD-causing mutations has allowed for experimental models which have proven integral to the overall understanding of AD2. However, the failure of pathology-targeting therapeutic development suggests that the formation of plaques and tangles may be symptomatic and not describe the etiology of the disease3,4. Here, we use an integrative, multi-omics approach and systems-level analysis in hiPSC-derived neurons to generate a mechanistic disease model for EOFAD. Using patient-specific cells from donors harboring mutations in PSEN1 differentiated into neurons, we characterize the disease-related gene expression and chromatin accessibility changes by RNA- Seq, ATAC-Seq, and histone methylation ChIP-Seq. We show that the defining disease-causing mechanism of EOFAD is dedifferentiation, primarily through the REST-mediated repression of neuronal lineage specification gene programs and the activation of non-specific germ layer precursor gene programs concomitant with modifications in chromatin accessibility. These gene signature profiles and changes in chromatin topology illustrate that EOFAD neurons traverse the chromatin landscape from an ectodermal origin to a mixed germ lineage state. Further, a reanalysis of existing transcriptomic data from PSEN1 patient brain samples demonstrates that the mechanisms identified in our experimental system recapitulate EOFAD in the human brain. Our results comprise a disease model which describes the mechanisms culminating in dedifferentiation that precede amyloid and tau pathology formation and engender neurodegeneration.

Impacts of Drugs on Alzheimer’s Diseases

2021 ◽  
Vol 7 (3) ◽  
Author(s):  
Bharti R ◽  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Review Article ◽  
Older Person ◽  
Disease Treatment ◽  
Mental Functions ◽  
Treatment Techniques ◽  
Alois Alzheimer ◽  
Alzheimer’S Diseases ◽  
Alzheimer's Diseases

In 1901, Alois Alzheimer first reported Alzheimer’s disease. It is a disease that destroys memory and other essential mental functions mostly observed in an older person and mainly in women. Various treatment techniques have been used, which involve Ayurveda, homeopathy, modern drugs, etc. Turmeric, Ashwagandha, Brahmi, Ghrita, etc. are some ayurvedic medicines used to cure this disease, but they were relatively slow in processing. Drugs like Donepezil, Galantamine, and Rivastigmine are speedy, and thus they are in the market nowadays. In this review article, we will give information and awareness about the drugs therapy used for disease treatment and their effects.

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