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

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

2020 ◽  
Vol 21 (21) ◽  
pp. 8338
Author(s):  
Kimberley D. Bruce ◽  
Maoping Tang ◽  
Philip Reigan ◽  
Robert H. Eckel

Lipoprotein lipase (LPL) is a key enzyme in lipid and lipoprotein metabolism. The canonical role of LPL involves the hydrolysis of triglyceride-rich lipoproteins for the provision of FFAs to metabolic tissues. However, LPL may also contribute to lipoprotein uptake by acting as a molecular bridge between lipoproteins and cell surface receptors. Recent studies have shown that LPL is abundantly expressed in the brain and predominantly expressed in the macrophages and microglia of the human and murine brain. Moreover, recent findings suggest that LPL plays a direct role in microglial function, metabolism, and phagocytosis of extracellular factors such as amyloid- beta (Aβ). Although the precise function of LPL in the brain remains to be determined, several studies have implicated LPL variants in Alzheimer’s disease (AD) risk. For example, while mutations shown to have a deleterious effect on LPL function and expression (e.g., N291S, HindIII, and PvuII) have been associated with increased AD risk, a mutation associated with increased bridging function (S447X) may be protective against AD. Recent studies have also shown that genetic variants in endogenous LPL activators (ApoC-II) and inhibitors (ApoC-III) can increase and decrease AD risk, respectively, consistent with the notion that LPL may play a protective role in AD pathogenesis. Here, we review recent advances in our understanding of LPL structure and function, which largely point to a protective role of functional LPL in AD neuropathogenesis.


2005 ◽  
Vol 15 ◽  
pp. S217
Author(s):  
T.V. Davidova ◽  
V.G. Fomina ◽  
N.I. Voskresenskaya ◽  
L.A. Vetrile ◽  
N.A. Trekova ◽  
...  

2018 ◽  
Vol 129 (4) ◽  
pp. 325-336 ◽  
Author(s):  
Guang Fang ◽  
Baoyan Shi ◽  
Kefeng Wu ◽  
Siyu Chen ◽  
Xiang Gao ◽  
...  

2000 ◽  
Vol 21 ◽  
pp. 23 ◽  
Author(s):  
Alon Monsonego ◽  
Ruth Maron ◽  
Amit Bar-Or ◽  
Jeff I. Krieger ◽  
Dennis Selkoe ◽  
...  

2011 ◽  
Vol 2011 ◽  
pp. 1-11 ◽  
Author(s):  
Elena Caldarazzo Ienco ◽  
Costanza Simoncini ◽  
Daniele Orsucci ◽  
Loredana Petrucci ◽  
Massimiliano Filosto ◽  
...  

Mitochondria, the powerhouse of the cell, play a critical role in several metabolic processes and apoptotic pathways. Multiple evidences suggest that mitochondria may be crucial in ageing-related neurodegenerative diseases. Moreover, mitochondrial haplogroups have been linked to multiple area of medicine, from normal ageing to diseases, including neurodegeneration. Polymorphisms within the mitochondrial genome might lead to impaired energy generation and to increased amount of reactive oxygen species, having either susceptibility or protective role in several diseases. Here, we highlight the role of the mitochondrial haplogroups in the pathogenetic cascade leading to diseases, with special attention to Alzheimer's disease.


2019 ◽  
Vol 15 ◽  
pp. P1292-P1292
Author(s):  
Timothy Daly ◽  
Anouk Barberbousse ◽  
Yves Agid ◽  
Stéphane Epelbaum

2015 ◽  
Vol 9 (5) ◽  
pp. 480 ◽  
Author(s):  
Ji Hyun Kim ◽  
Qian Wang ◽  
Ji Myung Choi ◽  
Sanghyun Lee ◽  
Eun Ju Cho

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