Role of Tau Protein in Neuronal Damage in Alzheimer's Disease and Down Syndrome

2012 ◽  
Vol 43 (8) ◽  
pp. 645-654 ◽  
Author(s):  
Ana M. Cárdenas ◽  
Alvaro O. Ardiles ◽  
Natalia Barraza ◽  
Ximena Baéz-Matus ◽  
Pablo Caviedes
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Down Syndrome ◽  
Tau Protein ◽  
Neuronal Damage

scholarly journals Polymorphisms inHSD17B1: Early Onset and Increased Risk of Alzheimer’s Disease in Women with Down Syndrome

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Joseph H. Lee ◽  
Susan Gurney ◽  
Deborah Pang ◽  
Alexis Temkin ◽  
Naeun Park ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Down Syndrome ◽  
Age At Onset ◽  
Nucleotide Polymorphisms ◽  
Risk Alleles ◽  
Increased Risk ◽  
Estrogen Activity ◽  
Intron 4

Background/Aims. Genetic variants that affect estrogen activity may influence the risk of Alzheimer's disease (AD). In women with Down syndrome, we examined the relation of polymorphisms in hydroxysteroid-17beta-dehydrogenase (HSD17B1) to age at onset and risk of AD.HSD17B1encodes the enzyme 17β-hydroxysteroid dehydrogenase (HSD1), which catalyzes the conversion of estrone to estradiol.Methods. Two hundred and thirty-eight women with DS, nondemented at baseline, 31–78 years of age, were followed at 14–18-month intervals for 4.5 years. Women were genotyped for 5 haplotype-tagging single-nucleotide polymorphisms (SNPs) in theHSD17B1gene region, and their association with incident AD was examined.Results. Age at onset was earlier, and risk of AD was elevated from two- to threefold among women homozygous for the minor allele at 3 SNPs in intron 4 (rs676387), exon 6 (rs605059), and exon 4 inCOASY(rs598126). Carriers of the haplotype TCC, based on the risk alleles for these three SNPs, had an almost twofold increased risk of developing AD (hazard ratio = 1.8, 95% CI, 1.1–3.1).Conclusion. These findings support experimental and clinical studies of the neuroprotective role of estrogen.

scholarly journals The role of calbindin‐D28k in a mouse model of Down syndrome‐related Alzheimer's disease

2020 ◽  
Vol 16 (S2) ◽  
Author(s):  
Eric D. Hamlett ◽  
Steven L. Carroll ◽  
Ann‐Charlotte Granholm
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Down Syndrome ◽  
Mouse Model ◽  
Calbindin D28k

Role of tau protein in Alzheimer's disease: The prime pathological player

2020 ◽  
Vol 163 ◽  
pp. 1599-1617 ◽  
Author(s):  
Shibi Muralidar ◽  
Senthil Visaga Ambi ◽  
Saravanan Sekaran ◽  
Diraviyam Thirumalai ◽  
Balamurugan Palaniappan
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Tau Protein

Recent Studies on Design and Development of Drugs Against Alzheimer’s Disease (AD) Based on Inhibition of BACE-1 and Other AD-causative Agents

2020 ◽  
Vol 20 (13) ◽  
pp. 1195-1213 ◽  
Author(s):  
Satya P. Gupta ◽  
Vaishali M. Patil
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Tau Protein ◽  
Protein Misfolding ◽  
Inhibition Mechanism ◽  
Design And Development ◽  
Causative Agents ◽  
Misfolding Disease ◽  
Structural Aspects

Background: Alzheimer’s disease (AD) is one of the neurodegenerative diseases and has been hypothesized to be a protein misfolding disease. In the generation of AD, β-secretase, γ-secretase, and tau protein play an important role. A literature search reflects ever increasing interest in the design and development of anti-AD drugs targeting β-secretase, γ-secretase, and tau protein. Objective: The objective is to explore the structural aspects and role of β-secretase, γ-secretase, and tau protein in AD and the efforts made to exploit them for the design of effective anti-AD drugs. Methods: The manuscript covers the recent studies on design and development of anti-AD drugs exploiting amyloid and cholinergic hypotheses. Results: Based on amyloid and cholinergic hypotheses, effective anti-AD drugs have been searched out in which non-peptidic BACE1 inhibitors have been most prominent. Conclusion: Further exploitation of the structural aspects and the inhibition mechanism for β-secretase, γ-secretase, and tau protein and the use of cholinergic hypothesis may lead still more potent anti-AD drugs.

Cysteine in Alzheimer's Disease

2020 ◽  
pp. 326-353
Author(s):  
Suvarna P. Ingale ◽  
Rupali Patil ◽  
Aman B. Upaganlawar
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Tau Protein ◽  
Protein Misfolding ◽  
Nitrosative Stress ◽  
Aβ Peptide ◽  
Abnormal Protein ◽  
Structural Part ◽  
Neurodegenerative Process

Alzheimer's disease (AD) is characterized by selective loss of neurons in the hippocampus and neocortex due to abnormalities in proteins, mainly Aβ peptide and tau protein, in the form of abnormal protein aggregations or depositions in neurons. Recently oxidative/nitrosative stress has been identified as an important facilitator of neurodegeneration in AD. Cysteine-dependent proteins are known to be associated with the neurodegenerative process. Such cysteine-dependent enzyme proteins are proteases, antioxidant enzymes, kinases, phosphatases, and also non-enzymatic proteins such that utilize cysteine as a structural part of the catalytic site. This chapter deals with the role of cysteine in handling reactive oxygen/nitrogen species during oxidative/nitrosative stress and posttranslational modification of proteins causing protein misfolding or protein aggregation during neurodegeneration associated with AD.

The role of neurovascular unit damage in the occurrence and development of Alzheimer’s disease

2019 ◽  
Vol 30 (5) ◽  
pp. 477-484 ◽  
Author(s):  
Xin Liu ◽  
DeRen Hou ◽  
FangBo Lin ◽  
Jing Luo ◽  
JingWen Xie ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Tau Protein ◽  
Senile Dementia ◽  
Neurovascular Unit ◽  
Common Type ◽  
Pathological Changes ◽  
Β Amyloid ◽  
Progressive Cognitive Impairment

Abstract Alzheimer’s disease (AD) is a neurodegenerative disease with progressive cognitive impairment. It is the most common type of senile dementia, accounting for 65%–70% of senile dementia [Alzheimer’s Association (2016). 2016 Alzheimer’s disease facts and figures. Alzheimers Dement. 12, 459–509]. At present, the pathogenesis of AD is still unclear. It is considered that β-amyloid deposition, abnormal phosphorylation of tau protein, and neurofibrillary tangles are the basic pathological changes of AD. However, the role of neurovascular unit damage in the pathogenesis of AD has been attracting more and more attention in recent years. The composition of neurovascular unit and the role of neurovascular unit damage in the occurrence and development of AD were reviewed in this paper.

Sign in / Sign up

Export Citation Format

Share Document