International Conference on
Alzheimers, Dementia and Related Neurodegenerative Diseases

Mutations in human protein DJ-1 cause an early onset of Parkinson’s disease. Reactive cysteine (Cys106) is crucial for the protective function of DJ-1, although the underlying mechanisms are unclear. We have found that a fraction of bacterially expressed hexahistidine tagged human DJ-1 eluted very slowly from Ni-NTA column with an apparent first order rate constant of ~10-4 s-1. This unusually tight binding was accompanied by the appearance of blue-violet color on Ni-NTA column. We demonstrate that Cys106 is carboxymethylated in a fraction of DJ-1 that binds tightly to Ni-NTA. However, when eluted protein was re-applied onto Ni-NTA column no tight binding has been observed indicating that the formation of high affinity complex with Ni-NTA depends on a transient modification of Cys106 residue that transforms into Cys106-carboxymethyl adduct upon elution from Ni-NTA. The formation of high affinity complexes and the appearance of blue color were also observed when Ni was replaced with Co, Cu or Zn. However, high affinity complexes were not formed when other affinity media such as iminodiacetic acid or carboxymethyl aspartate have been used instead of NTA. We conclude that an unknown metabolite reacts with Cys106 of DJ-1 to result in a relatively stable post-translational modification. This modification allows high affinity and high specificity interaction of DJ-1 with complexes of NTA with transition metals.

Hyung-Goo Kim is a Senior Scientist at Qatar Biomedical Research Institute. His current focus is in identifying new disease genes for neurological disorders to elucidate their underlying mechanism.

We report a genomic and phenotypic delineation for two chromosome regions with candidate genes for syndromic intellectual disability at 12q12 and Xp22.31. Fine mapping of six unreported small informative Copy Number Variations (CNVs) narrowed down the chromosomal interval to one gene LRRK2 at 12q12. Expression studies revealed high levels of LRRK2 transcripts in whole human brain, cerebral cortex and hippocampus. RT-qPCR assays revealed that LRRK2 transcripts were dramatically reduced in our micro deletion patient compared to his healthy grandfather with no deletion.

Jan Ricny is currently working in Department of Neurobiology at National Institute of Mental Health, Czech Republic. His research interest includes biochemistry of nervous system and its pathological conditions, cholinergic neurochemistry.

Statement of the problem: It is suggested that interactions of multifunctional mitochondrial protein 17β-hydroxysteroid dehydrogenase type 10 (17β-HSD10) and amyloid β (Aβ) peptides are involved in the pathogenesis of Alzheimer´s Disease (AD). In our previous research, we evaluated total levels of 17β-HSD10 and levels of 17β-HSD10 – Aβ complexes as prospective biomarkers for AD. In this study, we tried to evaluate the levels of 17β-HSD10 – Aβ1-42 with the aim to fi nd the better biomarker for AD than those available as yet.

Javier Sanchez is currently working as Head of Intensive Care Unit in Instituto Neurologia y Neurocirugia, Cuba. He has research interest in various fields which includes Stroke, Neurodegenerative disorders and Neurosurgery.

Ischemic stroke is a leading cause of disability, including post-stroke Cognitive Impairment (CI), for which no effective therapy is available. Post-stroke patients are managed with antiplatelet drugs and antihypertensive, hypoglycemic and/or cholesterol-lowering drugs, as needed. Policosanol is an antiplatelet and cholesterol-lowering agent. Previous studies demonstrated that adding Policosanol to Aspirin (AS) therapy improves post-stroke neurological recovery compared to placebo+AS. Policosanol effects on post-stroke CI have not been investigated yet.