Advanced glycation end products (AGEs) involvements in the development of frank Alzheimer’s disease (FAD)

糖基化 疾病 医学 老年学 内科学 内分泌学 糖尿病
作者
Vincent Oghenekevbe,O Olughor
出处
期刊:Alzheimers & Dementia [Wiley]
卷期号:20 (S8) 被引量:2
标识
DOI:10.1002/alz.095169
摘要

Abstract Background AGEs is one of the Maillard’s reaction products (MRPs) found in over‐processed common diets, causing food‐nutrients abnormal modifications. Some MRPs are potentially toxic or carcinogenic. MRPs present in stages: initial, intermediate and final. The aim of this presentation is to state roles played by AGEs in the development of AD as recent findings. Method Through threaded literature review Result 1) MRPs and disease causing associations were first recognized by Swedish scientists in 2002 and involvement of AGEs in development of AD in 2010; 2) MRPs include: N'fructoselysine (furosine), 5‐ Hydroxymethyl furfural (HMF), acrylamide, heterocyclic amines and melanoidins; 3) some neurotransmitters are modified amino acids, known as monoamines; 4) some other neurotransmitters are unmodified amino acids; 5) certain short chain amino acids (peptides) function as neuromodulators, by being able to alter a neuron’s response to a neurotransmitter, or block its release; 6) a neurotransmitter’s effect depends upon its concentration, the types and numbers of receptors and ion channels on the receiving cells' membranes; 7) neurotransmitters affect each other’s levels, the same neurotransmitter can even have opposite effects on different types of cells; 8) AD is due to depleted Acetylcholine (Ach) neurotransmitter in the brain, causing imbalance. Ach coordinates functions in the brain by enhancing nerve transmission in a horizontal direction and also inhibiting transmission in a vertical direction; 9) Ach can both inhibit and stimulate because it can bind two types of receptors: on basket cells (to decrease levels of GABA production and stimulate horizontal nerve transmission) and on bipolar cells (to increase GABA production and strengthen the inhibition of vertical transmission). Conclusion How AGEs disrupts some of these functions to contribute to the development of AD (typified by ‘forgetfulness and difficult‐thinking’) will be discussed.
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