scholarly journals Apolipoprotein E Polymorphism and Alzheimer’s Risk in Kashmiri Population

2021 ◽  
Vol 18 (4) ◽  
pp. 673-680
Author(s):  
Kamran Nissar ◽  
Arshad Hussain ◽  
Bashir Ahmad Ganai
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Gene Polymorphism ◽  
Apoe Gene ◽  
Gene Variation ◽  
Variant Genotype ◽  
Apolipoprotein E Polymorphism ◽  
Survey Results ◽  
Kashmiri Population

Background: Although the cause of Alzheimer's disease is unknown, most experts feel that the disease is caused by a combination of circumstances rather than a single cause. Age, gene polymorphism, diabetes, and other conditions are all risk factors for Alzheimer's disease. Given the importance of gene polymorphism in different diseases, we intended to find out the association of APOE gene polymorphism with Alzheimer's risk in the Kashmiri population. Method: Out of 300 patients who were referred to the memory clinic of the hospital, to evaluate the probable relation of APOE gene variation in Alzheimer's disease, we conducted the study on 59 clinically confirmed Alzheimer's patients and 52 age and ethnicity-matched healthy controls found in a community survey. Results: Our data revealed a statistically significant association of ε4 variant genotype of the APOE gene with AD susceptibility in the Kashmiri population. Conclusions: The current study's findings provided insight into the role of APOE polymorphisms in Alzheimer's disease susceptibility. The identified susceptibility variant may become a marker genotype for AD.

The Application Value of ApoE Gene Polymorphism in Alzheimer's Disease

2019 ◽  
Vol 9 (10) ◽  
pp. 1403-1407
Author(s):  
Cong Chen ◽  
Yuhui Zhang ◽  
Bin Chen ◽  
Chaosheng Zeng ◽  
Min Chen ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Gene Polymorphism ◽  
Apoe Genotype ◽  
Apoe Gene ◽  
Control Group ◽  
Apolipoprotein E Polymorphism ◽  
Abnormal Lipid Metabolism ◽  
And Control ◽  
Apoe Gene Polymorphism

To explore the association of apolipoprotein E polymorphism with Alzheimer's disease (AD), so as to provide possible research value for potential targeted therapy. 120 AD patients and 50 healthy volunteers were enrolled to extract fasting blood samples. ApoE gene polymorphism and blood lipids were tested in blood. ApoE gene and genotype frequency between AD group and control group were compared by PCR and sequencing methods. MMSE, CDR, and BPSD were used to determine the intelligence. ApoE genotype was detected by DNA microarray. ɛ4 carrier accounted for 45% in AD group, which was significantly elevated compared with control group (12%) (P < 0.05). TG, TC, and LDL-C levels were increased, while HDL-C was reduced in ɛ4 allele carriers (allP < 0.05). The MMSE scores of ApoEɛ4 genotype carriers in AD group were markedly lower than those of nonApoEɛ4 genotype carriers (P < 0.05) and control (P < 0.01). The proportion of dementia in ApoEɛ4 genotype carriers from AD group was apparently higher than the ɛ4 gene non-carriers (P < 0.05). The ApoEɛ4 gene is an AD risk factor. The changes of genotype and frequency of ApoEɛ4 gene are the main factors leading to abnormal lipid metabolism in AD patients, suggesting that ApoEɛ4 gene detection might be helpful for the early diagnosis and treatment of AD.

scholarly journals APOE GENE POLYMORPHISM: THE IMPACT OF APOE4 ALLELE ON SYSTEMIC INFLAMMATION AND ITS ROLE IN THE PATHOGENESIS OF ALZHEIMER’S DISEASE

2018 ◽  
Vol 20 (3) ◽  
pp. 303-312 ◽  
Author(s):  
I. K. Malashenkova ◽  
S. A. Krynskiy ◽  
M. V. Mamoshina ◽  
N. A. Didkovskiy
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Gene Polymorphism ◽  
Systemic Inflammation ◽  
Apoe Gene ◽  
Apoe4 Allele ◽  
The Impact ◽  
Apoe Gene Polymorphism

Interferon Gamma +874 T/A Gene Polymorphism is not a Risk Factor in the Pathogenesis of Alzheimer’s Disease

2009 ◽  
Vol 24 (S1) ◽  
pp. 1-1 ◽  
Author(s):  
A. Juhász ◽  
Á. Fehér ◽  
Á. Rimanóczy ◽  
J. Kálmán ◽  
Z. Janka
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Risk Factor ◽  
Gene Polymorphism ◽  
Interferon Gamma ◽  
Amyloid Beta ◽  
Simultaneous Occurrence ◽  
Healthy Controls ◽  
Inflammatory Processes

Inflammatory processes seem to play a role in neurodegenerative diseases such as Alzheimer's disease (AD). Local inflammatory mechanisms can affect to neurotoxicity, interfere with beta amyloid expression and metabolism. The increased production of amyloid precursor protein eventually leads to the deposition of amyloid beta. Interferon (INF) gamma plays a pivotal role in the inflammatory processes.The aim of this study was to evaluate the putative role of INF gamma +874 T/A polymorphism and its association with apolipoprotein E (ApoE) 4 allele in AD.One hundred and eighty nine healthy controls (HC) and 191 patients with AD were involved in this study. The probable AD patients were diagnosed by NINCDS-ADRDA criteria. The DNA was extracted from whole peripheral blood. INF gamma +874 T/A and ApoE polymorphisms were assessed by the PCR based method.ApoE 4 allele occurrence in AD was 27% compared to 9% in HC. There were no statistically significant differences in the distribution of INF gamma genotypes (AD: A/A:30.9%, T/A:46.1%, T/T:23.0%; HC: A/A:21.7%, T/A:54.5%, T/T:23.8%, p=0.110) or alleles. The INF gamma A/A genotype was more frequent in the presence of ApoE 4 allele in AD (13.6%) than in the HC (4.8%).Our results confirm the role of ApoE 4 allele in AD. However, no association was found between the INF gamma +874 T /A polymorphism and AD. The simultaneous occurrence of ApoE 4 allele and one of the INF gamma genotypes presumably can not modify the risk for AD. (ETT 198/04/2006 and OTKA K 60589/2006).

P.1.a.008 The role of the dopamine beta-hydroxylase gene polymorphism in Alzheimer's disease

2011 ◽  
Vol 21 ◽  
pp. S241
Author(s):  
A. Juhász ◽  
A. Fehér ◽  
M. Pákáski ◽  
J. Kálmán ◽  
Z. Janka
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Gene Polymorphism ◽  
Dopamine Beta Hydroxylase ◽  
Hydroxylase Gene

scholarly journals A CROSS-SECTIONAL ANALYSIS OF APOE GENE POLYMORPHISM AND THE RISK OF COGNITIVE IMPAIRMENTS IN THE ALZHEIMER’S DISEASE NEUROIMAGING INITIATIVE STUDY

2021 ◽  
pp. 1-6
Author(s):  
G. Wang ◽  
D.E. Vance ◽  
W. Li
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Gene Polymorphism ◽  
Cognitive Impairments ◽  
Apoe Genotype ◽  
Apoe Gene ◽  
Dependent Manner ◽  
Cross Sectional ◽  
Apoe Genotypes ◽  
Apoe Gene Polymorphism

Background: It is inconclusive on how apolipoprotein epsilon (APOE) gene polymorphism is associated with the risk of having mild cognitive impairment (MCI) or Alzheimer’s disease (AD). Objectives: To investigate how APOE genotype is associated with the risk of MCI or AD using the data collected from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) participants. Methods: A cross-sectional design was used to analyze the baseline data collected from the 1,720 ADNI participants. APOE gene polymorphism was analyzed on how they are related to the risk of cognitive impairments of either MCI or AD using a percent yield (PY) method. Then cognitive functions were compared among six different APOE genotypes using a two-way ANCOVA by controlling possible confounding factors. Results: The prevalence of six APOE genotypes in 1,720 participants is as following: e2/e2 (0.3%), e2/e3 (7.4%), e3/e3 (45.4%), e2/e4 (2%), e3/e4 (35%) and e4/e4 (9.9%). The e2/e2 and e4/e4 genotypes were associated with the lowest and the highest risk respectively for cognitive impairments of either MCI or AD. Further, a worse cognitive diagnosis was associated with an increasing number of APOE e4 allele in a dose dependent manner. Participants with genotype e3/e3 had a better memory measure than those with the genotype of e3/e4. Conclusions: APOE gene polymorphism is associated with different level of risks for cognitive impairments. The heterozygous genotype e3/e4 is associated with a worse memory function compared to the genotype of e3/e3. Further investigations are needed to intervene the cognitive deteriorations in those with at risk APOE genotypes.

scholarly journals Neuroprotection and Neurodegeneration in Alzheimer’s Disease: Role of Cardiovascular Disease Risk Factors, Implications for Dementia Rates, and Prevention with Aerobic Exercise in African Americans

2012 ◽  
Vol 2012 ◽  
pp. 1-14 ◽  
Author(s):  
Thomas O. Obisesan ◽  
Richard F. Gillum ◽  
Stephanie Johnson ◽  
Nisser Umar ◽  
Deborah Williams ◽  
...  
Keyword(s):  
Risk Factors ◽  
Alzheimer’S Disease ◽  
Cardiovascular Disease ◽  
Alzheimer's Disease ◽  
African Americans ◽  
Aerobic Exercise ◽  
The United States ◽  
Apoe Gene ◽  
Cvd Risk

Prevalence of Alzheimer’s disease (AD) will reach epidemic proportions in the United States and worldwide in the coming decades, and with substantially higher rates in African Americans (AAs) than in Whites. Older age, family history, low levels of education, and ɛ4 allele of the apolipoprotein E (APOE) gene are recognized risk factors for the neurodegeneration in AD and related disorders. In AAs, the contributions of APOE gene to AD risk continue to engender a considerable debate. In addition to the established role of cardiovascular disease (CVD) risk in vascular dementia, it is now believed that CVD risk and its endophenotype may directly comediate AD phenotype. Given the pleiotropic effects of APOE on CVD and AD risks, the higher rates of CVD risks in AAs than in Whites, it is likely that CVD risks contribute to the disproportionately higher rates of AD in AAs. Though the advantageous effects of aerobic exercise on cognition is increasingly recognized, this evidence is hardly definitive, and data on AAs is lacking. In this paper, we will discuss the roles of CVD risk factors in the development of AD and related dementias, the susceptibility of these risk factors to physiologic adaptation, and fitness-related improvements in cognitive function. Its relevance to AD prevention in AAs is emphasized.

Dissecting the role of Corticotropin-releasing hormone receptor type 1 in Alzheimer's Disease

2011 ◽  
Vol 44 (06) ◽  
Author(s):  
K Lerche ◽  
M Willem ◽  
K Kleinknecht ◽  
C Romberg ◽  
U Konietzko ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Hormone Receptor ◽  
Receptor Type ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone

Role of melatonin in regulating neurogenesis: Implications for the neurodegenerative pathology and analogous therapeutics for Alzheimer’s disease

2020 ◽  
Vol 3 (2) ◽  
pp. 216-242 ◽  
Author(s):  
Mayuri Shukla ◽  
Areechun Sotthibundhu ◽  
Piyarat Govitrapong
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Adult Neurogenesis ◽  
Adult Brain ◽  
Therapeutic Approaches ◽  
Therapeutic Implications ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
Progenitor Cell Proliferation

The revelation of adult brain exhibiting neurogenesis has established that the brain possesses great plasticity and that neurons could be spawned in the neurogenic zones where hippocampal adult neurogenesis attributes to learning and memory processes. With strong implications in brain functional homeostasis, aging and cognition, various aspects of adult neurogenesis reveal exuberant mechanistic associations thereby further aiding in facilitating the therapeutic approaches regarding the development of neurodegenerative processes in Alzheimer’s Disease (AD). Impaired neurogenesis has been significantly evident in AD with compromised hippocampal function and cognitive deficits. Melatonin the pineal indolamine augments neurogenesis and has been linked to AD development as its levels are compromised with disease progression. Here, in this review, we discuss and appraise the mechanisms via which melatonin regulates neurogenesis in pathophysiological conditions which would unravel the molecular basis in such conditions and its role in endogenous brain repair. Also, its components as key regulators of neural stem and progenitor cell proliferation and differentiation in the embryonic and adult brain would aid in accentuating the therapeutic implications of this indoleamine in line of prevention and treatment of AD.   

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