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Page 4 of 24 Neuroimmunol Neuroinflammation 2019;6:15 I http://dx.doi.org/10.20517/2347-8659.2019.019

In rare cases, a chronic granulomatous process may lead to formation of a mass lesion (cryptococcoma)
that has a tumoral appearance. Metabolites released by cryptococcus can inhibit the migration and function
of leukocytes and promote survival and localized replication of the pathogen, thus facilitating chronic
granulomatous inflammation and giant cryptococcoma formation.

5. Analysis of repetitive element expression in the blood and skin of patients with parkinson’s
disease identifies differential expression of satellite elements

Kimberley J. Billingsley, Freddy Lättekivi, Anu Planken, Ene Reimann, Lille Kurvits, Liis
Kadastik-Eerme, Kristjan M. Kasterpalu, Vivien J. Bubb, John P. Quinn, Sulev Kõks, Pille Taba

Perron Institute for Neurological and Translational Science, Sarich Neuroscience Research Institute; Centre for
Comparative Genomics, Murdoch University, Murdoch, Western Australia, Australia

Repetitive elements (RE) constitute the majority of the human genome and have a range of functions both
structural and regulatory on genomic function and gene expression. RE overexpression has been observed
in several neurodegenerative diseases, consistent with the observation of aberrant expression of RE posing
a mutagenic threat. Despite reports that associate RE expression with Parkinson’s disease (PD) no study has
comprehensively analysed the role of these elements in the disease. This study presents the first genome-
wide analysis of RE expression in PD to date. Analysis of RNA-sequencing data of 12 PD patients and
12 healthy controls identified tissue-specific expression differences and more significantly, differential
expression of four satellite elements; two simple satellite III (repName = CAttC_nand_GAATG_n) a
high-copy satellite II (HSATII) and a centromeric satellite (ALR_Alpha) in the blood of PD patients. In
support of the growing body of recent evidence associating REs with neurodegenerative disease, this study
highlights the potential importance of characterization of RE expression in such diseases.

6. Alzheimer’s disease: is the inflammasome the missing link?

2
3
1
Elaine Chan Wan Ling , Gan Sook Yee , Benjamin Simon Pickard
1 Institute for Research, Development and Innovation, International Medical University, Kuala Lumpur 57000,
Malaysia
2 School of Pharmacy, International Medical University, Kuala Lumpur 57000, Malaysia
3 Strathclyde Institute of Pharmacy and Biomedical Sciences, University of Strathclyde, Glasgow, G4 0RE, UK

Alzheimer’s disease (AD) is a devastating neurodegenerative disease characterised by widespread neuronal
cell death and progressive dementia. Genetic and molecular studies have confirmed the central role of
amyloid-β (Aβ) production in the pathogenesis of AD. However, therapies eliminating Aβ from AD have
unfortunately failed to stem progressive cognitive decline. The association of several immune responsive
genes with increased AD risks have in recent years revealed that inflammatory mechanisms are also a
powerful pathogenic forces in the process of neurodegeneration.

Inflammasome, a multiprotein complex, is implicated in the execution of inflammatory responses and
pyroptotic death leading to neurodegeneration. Inflammasomes serve as platforms for the recruitment
and activation of caspase-1, the de facto executioner of a diverse downstream inflammatory processes