Accumulation of AGEs leads to tissue damage via alteration of the structures and functions of tissue proteins, stimulation of cellular responses, through receptors specific for AGE-proteins, and generation of reactive oxygen intermediates. AGEs also react with DNA, thus causing mutations and DNA transposition. Thermal processing of proteins and carbohydrates brings major changes in allergenicity. AGEs are antigenic and represent many of the important neoantigens found in cooked or stored foods. They also interfere with the normal product of nitric oxide in cells.Although there are several lysine and arginine residues in the serum albumin structure, very few of them can take part in the glycation reaction. Oxidation
The albumin is the predominant protein in most body fluids, its Cys34 represents the largest fraction of free thiols within body. The albumin Cys34 thiol exists in both reduced and oxidized forms. In plasma of healthy young adults, 70–80% of total HSA contains the free sulfhydryl group of Cys34 in a reduced form or mercaptoalbumin (HSA-SH). However, in pathological states characterized by oxidative stress and during the aging process, the oxidized form, or non-mercaptoalbumin (HNA), could predominate. The albumin thiol reacts with radical hydroxyl (.OH), hydrogen peroxide (H2O2) and the reactive nitrogen species as peroxynitrite (ONOO. ), and have been shown to oxidize Cys34 to sulfenic acid derivate (HSA-SOH), it can be recycled to mercapto-albumin; however at high concentrations of reactive species leads to the irreversible oxidation to sulfinic (HSA-SO2H) or sulfonic acid (HSA-SO3H) affecting its structure.
Finally in a review in 1995 Demirkiran and Jankovic stated the disease should be called paroxysmal kinesigenic dyskinesia instead, pointing out that the attacks could manifest as any form of dyskinesia, not just choreoathetosis. See also
Paroxysmal dyskinesia
Paroxysmal nonkinesogenic dyskinesia
Paroxysmal exercise-induced dystonia

References
External links

GeneReviews/NIH/NCBI/UW entry on Familial Paroxysmal Kinesigenic Dyskinesia
OMIM entries on Familial Paroxysmal Kinesigenic Dyskinesia