d-ribose and pathogenesis of Alzheimer's disease

被引:19
作者
Javed, Mehjbeen [1 ]
Ahmad, Md. Irshad [2 ,3 ]
Javed, Hina [4 ]
Naseem, Sufia [5 ]
机构
[1] Aligarh Muslim Univ, Dept Zool, Aquat Toxicol Res Lab, Aligarh, IP, India
[2] Aligarh Muslim Univ, Fac Life Sci, Dept Biochem, Aligarh, IP, India
[3] All India Inst Med Sci, Dept Biophys, New Delhi 110029, India
[4] Aligarh Muslim Univ, Dept Chem, Aligarh, UP, India
[5] Aligarh Muslim Univ, Fac Med, Dept Biochem, Aligarh, UP, India
关键词
AGE; Alzheimer's; Amyloid beta; d-ribose; Glycation; RAGE; Tau; GLYCATION END-PRODUCTS; AMYLOID-BETA; TAU HYPERPHOSPHORYLATION; MAILLARD REACTION; PROTEIN; CELL; PERFORMANCE; PRECURSOR; PATHOLOGY; STRESS;
D O I
10.1007/s11033-020-05243-7
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
It is estimated that the global prevalence of dementia will rise as high as 24 million and predicted to be double in every 20 years which is attributed to the fact that the ageing population is increasing and so more individuals are at risk of developing neurodegenerative diseases like Alzheimer's. Many scientists favored glycation of proteins such as tau, amyloid beta (A beta) etc. as one of the important risk factor in Alzheimer's disease (AD). Since, d-ribose shows highest glycation ability among other sugars hence, produces advanced glycation end products (AGEs) rapidly. However, there are several other mechanisms suggested by researchers through which d-ribose may cause cognitive impairments. There is a concern related to diabetic patients since they also suffer from d-ribose metabolism, may be more prone to AD risk. Thus, it is imperative that the pathogenesis and the pathways involved in AD progression are explored in the light of ribosylation and AGEs formation for identifying suitable diagnostics marker for early diagnosis or finding promising therapeutic outcomes.
引用
收藏
页码:2289 / 2299
页数:11
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