Association of polymorphisms in the LRP1 and A2M genes with Alzheimer’s disease in the Northern Chinese Han population

Yuan, Quan; Wang, Fen; Xue, Sufang; Jia, Jianping

doi:10.1016/j.jocn.2012.01.052

Cited by 10 publications

(6 citation statements)

References 23 publications

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“… First author Year Country Ethnicity AD Controls Criteria for AD diagnosis Genotyping method Source of control Time of AD onset Quality score N a Age b Age c Gender d N Age b Gender d Yuan, Q. 50 2013 China Asian 364 74.9 69.9 57% 291 73.7 60% NINCDS-ADRDA PCR and Direct sequencing HB Mixed 9 Vargas, T. 32 2010 Spain Caucasian 746 NA 73.7 66% 598 74.8 68% NINCDS-ADRDA and DSM-IV TaqMan SNP Genotyping Assays PB NA 12 Vazquez-Higuera, J. L. 52 2009 Spain Caucasian 246 76.6 72.9 65% 237 81.2 69% NINCDS-ADRDA PCR-RFLP PB Mixed 10 Chen, Y. 29 2009 China Asian 67 71.9 NA 34% 77 70.0 45% NINCDS-ADRDA PCR-RFLP PB NA 8 Bahia, V. S. 33 …”

Section: Resultsmentioning

confidence: 99%

“… First author AD Control HWE CC CT TT C T CC CT TT C T P a Yuan, Q. 50 304 54 6 662 66 232 52 7 516 66 0.058 Vargas, T. 32 559 172 15 1290 202 442 138 18 1022 174 0.079 Vazquez-Higuera, J. L. 52 193 51 2 437 55 198 35 4 431 43 0.107 Chen, Y. 29 59 8 0 126 8 56 19 2 131 23 0.800 Bahia, V. S. 33 87 28 5 202 38 86 30 4 202 38 0.497 Rodriguez, E. 34 211 NA NA NA NA 233 NA NA NA NA 0.576 Forero, D.A.…”

Section: Resultsmentioning

confidence: 99%

“…Some studies consider that the LRP1 C766T polymorphism might be responsible for susceptibility to AD by interact with other genes, such as APOE 48 – 51 , MAPT 52 , and MAPK8IP1 53 . In addition, some speculated that LRP1 C766T may be in linkage disequilibrium with a deleterious mutation in the LRP1 gene, or with other biologically relevant mutation on neighbouring genes, which affected LRP1 expression 44 , 50 . Besides, several studies have a hypothesis that the LRP1 C766T polymorphism might alter the secondary structure of the LRP mRNA to affect the translation and stability of the protein 13 , 48 .…”

Section: Discussionmentioning

confidence: 99%

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Association between LRP1 C766T polymorphism and Alzheimer’s disease susceptibility: a meta-analysis

Wang

Liu

Wang³

et al. 2017

Sci Rep

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Low density lipoprotein receptor-related protein 1 (LRP1) C766T polymorphism (rs1799986) has been extensively investigated for Alzheimer’s disease (AD) susceptibility. However, results in different studies have been contradictory. Therefore, we conducted a meta-analysis containing 6455 AD cases and 6304 controls from 26 independent case–control studies to determine whether there was an association between the LRP1 C766T polymorphism and AD susceptibility. The combined analysis showed that there was no significant association between LRP1 C766T polymorphism and AD susceptibility (TT + CT versus CC: OR = 0.920, 95% CI = 0.817–1.037, P = 0.172). In subgroup analysis, significant decreased AD susceptibility was found among Asian population in allele model (T versus C: OR = 0.786, 95% CI = 0.635–0.974, P = 0.028) and dominant model (TT + CT versus CC: OR = 0.800, 95% CI = 0.647–0.990, P = 0.040). Moreover, T allele of LRP1 C766T was statistically associated with late onset of AD (LOAD) (T versus C: OR = 0.858, 95% CI = 0.748–0.985, P = 0.029; TT + CT versus CC: OR = 0.871, 95% CI = 0.763–0.994, P = 0.040). In conclusion, our meta-analysis suggested that LRP1 C766T polymorphism was associated with lower risk of AD in Asian, and could reduce LOAD risk especially. Considering some limitations of our meta-analysis, further large-scale studies should be done to reach a more comprehensive understanding.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Association between LRP1 C766T polymorphism and Alzheimer’s disease susceptibility: a meta-analysis

Wang

Liu

Wang³

et al. 2017

Sci Rep

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“…In addition, specialized neuronal proteins such as amyloid precursor protein (APP), the Aβ peptide, neurofibrillary tangles, Tau proteins, and amyloid plaques are plays a role in the alteration of neuronal function and its enhance the neurodegeneration and development of AD [50,51]. Furthermore, these changes are due to alteration of multiple cellular signaling cascades such as over activation of α, β and γ secretase; beta-site APP-cleaving enzyme 1 and 2 (BACE 1 & BACE 2 ); presenilins proteins 1 and 2 (P 1 & P 2 ); apolipoprotein E-epsilon4 variant (ApoE-ε4); alpha 2 -macroglobulin; and calcium dependent kinases [49, [52][53][54][55]. LPO and their metabolites contribute to the development of Role of Lipid Peroxidation Process in Neurodegenerative Disorders DOI: http://dx.doi.org/10.5772/intechopen.81188 neurovascular complication and neurodegeneration by activation of the above signaling pathways.…”

Section: Role Of Lpo In Alzheimer Diseasementioning

confidence: 99%

Role of Lipid Peroxidation Process in Neurodegenerative Disorders

Muthuraman¹,

Rishitha²,

Paramakrishnan³

et al. 2020

Lipid Peroxidation Research

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Lipid peroxidation is one of the primary events of the cell injury process. In pathophysiological condition, it is undergoing the initiation of organ damage. Various free radicals are playing a key role in this lipid peroxidation process. Free radical associated organ damage involves the three major phases, that is, initiation, propagation and termination. The primary source of various free radical formations is mediated through the pathophysiological function of mitochondria. Lipid peroxidation is contributed to the multiple neurodegenerative disorders. Thus, the various endogenous cellular anti-oxidant systems are regulated lipid peroxidation process and control the neurodegenerative action. Some of the molecules are targeted to attenuate the lipid peroxidation and their mediators for the prevention of neurodegeneration.

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“…The pathogenesis of AD is through the alteration of neuronal proteins, that is, amyloid precursor protein (APP), Aβ peptide that leads to the formation of neurofibrillary tangles, tau hyperphosphorylation, and amyloid plaques in the brain cortex and hippocampus regions . These changes are due to the actions of intracellular enzyme cascades, that is, secretase (α, β, and γ isotypes), beta-site APP-cleaving enzyme (BACE 1 and BACE 2 ), presenilins (P 1 and P 2 ), apolipoprotein E-epsilon 4 variant (ApoE-ε4), alpha 2 -macroglobulin, and abnormal activation of calcium dependent kinases (PKC, ERK 2 , Src, and RTK). − ACE metabolizes Aβ proteins that are responsible for the development of memory dysfunctions . However, overexpression of ACE in myelomonocytic cells alters the immune response, that causes amelioration of AD …”

Section: The Pharmacology Of Ace Inhibitors In Various Neurodegenerat...mentioning

confidence: 99%

The Implications of Angiotensin-Converting Enzymes and Their Modulators in Neurodegenerative Disorders: Current and Future Perspectives

Kaur

Muthuraman

Kaur

2015

ACS Chem. Neurosci.

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Angiotensin converting enzyme (ACE) is a dipeptidyl peptidase transmembrane bound enzyme. Generally, ACE inhibitors are used for the cardiovascular disorders. ACE inhibitors are primary agents for the management of hypertension, so these cannot be avoided for further use. The present Review focuses on the implications of angiotensin converting enzyme inhibitors in neurodegenerative disorders such as dementia, Alzheimer's disease, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, stroke, and diabetic neuropathy. ACE inhibitors such as ramipril, captopril, perindopril, quinapril, lisinopril, enalapril, and trandolapril have been documented to ameliorate the above neurodegenerative disorders. Neurodegeneration occurs not only by angiotensin II, but also by other endogenous factors, such as the formation of free radicals, amyloid beta, immune reactions, and activation of calcium dependent enzymes. ACE inhibitors interact with the above cellular mechanisms. Thus, these may act as a promising factor for future medicine for neurological disorders beyond the cardiovascular actions. Central acting ACE inhibitors can be useful in the future for the management of neuropathic pain due to following actions: (i) ACE-2 converts angiotensinogen to angiotensin(1-7) (hepatapeptide) which produces neuroprotective action; (ii) ACE inhibitors downregulate kinin B1 receptors in the peripheral nervous system which is responsible for neuropathic pain. However, more extensive research is required in the field of neuropathic pain for the utilization of ACE inhibitors in human.

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Association of polymorphisms in the LRP1 and A2M genes with Alzheimer’s disease in the Northern Chinese Han population

Cited by 10 publications

References 23 publications

Association between LRP1 C766T polymorphism and Alzheimer’s disease susceptibility: a meta-analysis

Association between LRP1 C766T polymorphism and Alzheimer’s disease susceptibility: a meta-analysis

Role of Lipid Peroxidation Process in Neurodegenerative Disorders

The Implications of Angiotensin-Converting Enzymes and Their Modulators in Neurodegenerative Disorders: Current and Future Perspectives

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