scholarly journals The role of ABCB1 and ABCA1 in beta-amyloid clearance at the neurovascular unit in Alzheimer's disease

2013 ◽  
Vol 4 ◽  
Author(s):  
Ayman ElAli ◽  
Serge Rivest
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neurovascular Unit ◽  
Beta Amyloid

The role of T cell reactivity to A-beta amyloid peptide in the pathogenic processes associated with Alzheimer's disease

2000 ◽  
Vol 21 ◽  
pp. 23 ◽  
Author(s):  
Alon Monsonego ◽  
Ruth Maron ◽  
Amit Bar-Or ◽  
Jeff I. Krieger ◽  
Dennis Selkoe ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
T Cell ◽  
Beta Amyloid ◽  
Amyloid Peptide ◽  
Cell Reactivity ◽  
Beta Amyloid Peptide ◽  
T Cell Reactivity

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.

scholarly journals P4-049: AN INTERNATIONAL BIBLIOMETRIC STUDY OVER 25 YEARS INTO THE ROLE OF BETA-AMYLOID IN ALZHEIMER'S DISEASE

2019 ◽  
Vol 15 ◽  
pp. P1292-P1292
Author(s):  
Timothy Daly ◽  
Anouk Barberbousse ◽  
Yves Agid ◽  
Stéphane Epelbaum
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Beta Amyloid ◽  
Bibliometric Study

scholarly journals Therapeutic Potential of Neu1 in Alzheimer’s Disease Via the Immune System

2021 ◽  
Vol 36 ◽  
pp. 153331752199614
Author(s):  
Aiza Khan ◽  
Sumit Das ◽  
Consolato Sergi
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Immune System ◽  
Therapeutic Potential ◽  
Amyloid Plaques ◽  
Beta Amyloid ◽  
Underlying Mechanism ◽  
Amyloid Deposits ◽  
Potential Therapeutic Role

Alzheimer’s Disease (AD) is pathologically characterized by the accumulation of soluble oligomers causing extracellular beta-amyloid deposits in form of neuritic plaques and tau-containing intraneuronal neurofibrillary tangles in brain. One proposed mechanism explaining the formation of these proteins is impaired phagocytosis by microglia/macrophages resulting in defective clearance of soluble oligomers of beta-amyloid stimulating aggregation of amyloid plaques subsequently causing AD. However, research indicates that activating macrophages in M2 state may reduce toxic oligomers. NEU1 mutation is associated with a rare disease, sialidosis. NEU1 deficiency may also cause AD-like amyloidogenic process. Amyloid plaques have successfully been reduced using NEU1.Thus, NEU1 is suggested to have therapeutic potential for AD, with lysosomal exocytosis being suggested as underlying mechanism. Studies however demonstrate that NEU1 may activate macrophages in M2 state, which as noted earlier, is crucial to reducing toxic oligomers. In this review, authors discuss the potential therapeutic role of NEU1 in AD via immune system.

scholarly journals Role of cathepsins in Alzheimer's disease: A systematic review

2018 ◽  
Vol 7 (1) ◽  
pp. 1-10
Author(s):  
S. Rastegar ◽  
A. Nouri ◽  
R. Masoudi ◽  
R. Tavakoli
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Final Analysis ◽  
Beta Amyloid ◽  
Protective Role ◽  
Biomedical Sciences ◽  
C Terminus ◽  
Apo E ◽  
The Subject

Alzheimer's disease (AD) is a multifactorial disease. In addition to the precipitating of two proteins betaamyloid peptide and neurofebrillary tangles, which are the main mechanisms involved in the pathogenesis ofAD, other factors such as inflammatory mechanisms and changes in lysosomal enzymes play an important part in the pathogenesis of this disease. Increased and decreased lysosomal proteases, such as cathepsin, can lead to functional impairment and gradual death of neurons. The aim of this review was to investigate the role of cathepsins in the pathogenesis of AD. To conduct this review, relevant articles published between 2000 and 2016, and indexed in reliable databases including PubMed, Google Scholar, Scopus and Web of Science were retrieved. After reviewing the articles, 30 articles that directly addressed the subject of this review were included in final analysis. Cathepsins exacerbate intracellular conditions in neurons, by processing beta-amyloid precursor protein and converting it into amyloid beta. They also play a protective role against AD and fight it by catalyzing the decomposition of beta-amyloids and converting them into the cut out forms of the carboxyl C-terminus. In addition, the 24 kDa fragment resulting from the effect of cathepsin D on apolipoprotein E (ApoE) is the second binding to the receptor in the ApoE. This fragment may also be the cause of the pathogenicity of Apo E in AD. Identifying and explaining the mechanisms involved in the pathogenesis of AD can play a significant role in the prevention and treatment of this disease. Since cathepsins play a pivotal role in the decomposition of beta-amyloid and reduction of the risk of AD, further studies can be considered an effective approach to study AD.Journal of Medical and Biomedical Sciences (2018) 7(1), 1 - 10

scholarly journals Inflammation in Alzheimer’s disease: A friend or foe?

2018 ◽  
Vol 5 (8) ◽  
pp. 2552-2564 ◽  
Author(s):  
Samaila Musa Chiroma ◽  
Mohamad Taufik Hidayat Baharuldin ◽  
Che Norma Mat Taib ◽  
Zulkhairi Amom ◽  
Saravanan Jagadeesan ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Beta Amyloid ◽  
Aβ Peptide ◽  
Cellular Mechanisms ◽  
Scientific Databases ◽  
Amyloid Aβ ◽  
The Brain ◽  
Convincing Data

Background: There is a dearth of precise information for molecular and cellular mechanisms responsible for the development of Alzheimer’s disease (AD). However, convincing data from clinical research and basic molecular biology have shown that inflammation of the brain is an integral part of AD. In this review, the role of inflammation in AD will be highlighted. Methods: Articles from credible scientific databases, such as ScienceDirect, Scopus, PubMed, Google Scholar and Mendeley, were searched and retrieved using keywords ‘inflammation’, ‘Alzheimer’s disease’, ‘tau’, and ‘beta amyloid’. Results: At present, there is no local inflammatory-inciting factor that is closely associated with AD, although it has been proposed that inflammation could be induced by pathologic hallmarks of AD, such as beta amyloid (Aβ) peptide plagues and neurofibrillary tangles (NFTs), or fragments of degenerated neurons. However, it is still unclear whether inflammation leads to the development of AD or if the pathological hallmarks of AD induce inflammation. Conclusion: Inflammation is, indeed, an integral part of AD. Further studies on inflammatory-targeted therapies for AD are highly recommended.

O1-03-01: Linking declining levels of plasma beta-amyloid 42 to Alzheimer's disease: The role of cerebral microbleeds

2013 ◽  
Vol 9 ◽  
pp. P129-P129 ◽  
Author(s):  
Adam Brickman ◽  
Irene Meier ◽  
Anne Wiegman ◽  
Vanessa Guzman ◽  
Jennifer Manly ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Beta Amyloid ◽  
Cerebral Microbleeds
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