Advances in Alzheimer's and Parkinson's Disease: Insights, by Abraham Fisher, Maurizio Memo, Fabrizio Stocchi, Israel

By Abraham Fisher, Maurizio Memo, Fabrizio Stocchi, Israel Hanin

Proceedings of the seventh foreign convention on Alzheimer’s disorder and Parkinson’s illness (ADPD), held March 9-13, 2005 in Sorrento, Italy.

The subject material of the ADPD meetings is exclusive in that it offers not just with concerns similar separately to Alzheimer’s sickness and Parkinson’s sickness, but additionally with the combination of those and different comparable ailments. the main up to date concepts and examine findings are illustrated during this quantity, protecting subject matters equivalent to immunology, neuroscience, pharmacology, genetics, molecular biology, biochemistry and the historical past, epidemiology, scientific phenomenology, prognosis, imaging, remedy ,and destiny views of Alzheimer’s and Parkinson’s Diseases.

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References 1. Marti TM, Kunz C, Fleck O. DNA mismatch repair and mutation avoidance pathways. J Cell Physiol 2002;191:28–41. 2. Liu B, Parson R, Papadopoulos N. Analysis of mismatch repair genes in hereditary nonpolyposis colorectal cancer patients. Nat Med 1996;2:169–174. 3. Eshelman JR, Markowitz SD. Mismatch repair defects in human carcinogenesis. Hum Mol Genet 1996;5:1489–1494. 4. Acharya S, Foster PL, Brooks P, Fischel R. The coordinated functions of the E. coli MutS and MutL proteins in mismatch repair.

These numbers are expected to increase. Regarding the functions of parkin protein, one of the most important functions is its enzymatic activity as a ubiquitin-protein ligase (E3) of the ubiquitin system [23]. The ubiquitin system consists of three enzymes: a ubiquitin-activating enzyme (E1), a ubiquitin-conjugating enzyme (E2), and a ubiquitinprotein ligase (E3). The ubiquitin-proteasome system (UPS) is an important intracellular proteolytic system responsible for a wide variety of biologically important cellular processes, such as cell cycle progression, signaling cascades, developmental programs, the protein quality control system, DNA repair, apoptosis, signal transduction, transcription, metabolism, immunity, and neurodegeneration.

PARK7 PARK7 is an autosomal recessive familial PD caused by mutations of DJ-1 [5], which has been mapped to the short arm of chromosome 1 at 1p36. To date, 6 missense mutations, 1 intronic mutation, 1 small deletion, and 2 exonic deletions (exons 1 to 5 and exons 5 to 7) have been identified [5,52–54]. DJ-1 mutations are rare compared with parkin and PINK1 mutations. We have not been able to find a DJ-1 mutation among Japanese families so far tested. DJ-1 was identified as a novel oncogene that transformed mouse NIH3T3 cells in cooperation with activated Ras, and mapped to 1p36 [55].

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