Search bioRxiv⌕ Search

Biology subjects

Vitic, Z.

Publications and source records attributed to Vitic, Z..

3 recordsLinked to original sources

Profiling peripheral immune cells in Parkinsons disease: A Scoping Review

Parkinsons disease (PD) is increasingly recognized as a multi-system disorder with immune dysregulation extending beyond the central nervous system. Although numerous studies have examined peripheral immune alterations in people with PD, findings remain heterogenous and difficult to reconcile. To clarify the current landscape, we conducted a comprehensive scoping review of human studies profiling peripheral blood immune cells in PD. Following PRISMA-ScR guidelines, we systematically screened the literature and curated studies reporting in vivo and ex vivo immune characterizations from PD patients. Eligible studies based on pre-defined criteria were assessed for patient demographics and clinical variables, experimental and analytical approaches, and reported immune outcomes. Our synthesis reveals a steady expansion and diversification of peripheral immune cell research in PD especially over the last decade. Deep immunophenotyping identifies convergent signatures across in vivo studies of both innate and adaptive compartments, including expanded pro-inflammatory T-cell subsets, altered monocyte subset distributions, increased cytotoxic natural killer cells and neutrophil-to-lymphocyte ratio, and dysregulated pathways related to immune activation, chemotaxis, mitochondrial function, and autophagy-lysosomal processes. Stimulation-based ex vivo assays further demonstrate recurrent T-cell hyper-responsiveness in PD, whereas myeloid cell responses are more variable and context dependent. Critically, this review highlights substantial variability and under-reporting in study design, which impeded our ability to make strong conclusions relating to many aspects of PD peripheral immunity.

immunology↗

Abundant non-inclusion α-synuclein pathology in Lewy body-negative LRRK2-mutant cases

Lewy body diseases are common neurodegenerative diseases, including Parkinsons disease (PD) and dementia with Lewy bodies, which lead to both motor and non-motor symptoms. They are neuropathologically characterized by loss of neuromelanized neurons in the substantia nigra pars compacta and -synuclein-immunopositive inclusions (Lewy bodies) in several types of neurons in the brain. A fraction of monogenic PD cases, however, represent a conundrum, as they can present with clinical Lewy body disease but do not have Lewy bodies upon neuropathological examination. For LRRK2, the presence or absence of Lewy bodies is not related to any specific mutation in the gene and different clinical presentation and neuropathology can be present even in the same family. Here, we present the first evidence of widespread -synuclein accumulation detected with proximity ligation assay (PLA) using the MJFR14-6-4-2 antibody in six Lewy body-negative LRRK2 cases and compare the levels with five patients with neuropathologically-verified Lewy body disease and six healthy controls. We show that non-inclusion aggregated -synuclein in the form of particulate PLA signal is dominant in the LRRK2 cases, while both Lewy-like and particulate PLA signal is found in late-stage Lewy body disease. Furthermore, LRRK2 cases displayed prominent particulate PLA signal in pontocerebellar tracts and inferior olivary nuclei in the brainstem, which was not seen in idiopathic Lewy body disease cases. These results suggest that Lewy-body negative LRRK2-related PD is not associated with a lack of -synuclein aggregation in neurons but rather a deficiency in the formation of inclusions.

neuroscience↗

MJF-14 proximity ligation assay detects early non-inclusion alpha-synuclein pathology with enhanced specificity and sensitivity

Lewy pathology, consisting of Lewy bodies and Lewy neurites, is the pathological hallmark of synucle-inopathies such as Parkinsons disease and dementia with Lewy bodies, but it is generally thought to represent late-stage pathological changes. In contrast, -synuclein oligomers are regarded as early-stage pathology, likely involved in disease progression and cellular toxicity. Oligomers, however, are not de-tected by standard immunohistochemistry but require specific detection techniques such as the proxim-ity ligation assay (PLA). Here, we describe the MJF-14 PLA, a new PLA towards aggregated -synuclein with unprecedented specificity, attained by the utilization of aggregate conformation-specific -synu-clein antibody MJFR-14-6-4-2 (hereafter MJF-14). Signal in the assay directly correlates with -synuclein aggregation in SH-SY5Y cells, as treatment with aggregation inhibitor ASI1D significantly lowers PLA sig-nal. In human cortical neurons, MJF-14 PLA detects pre-formed fibril-induced aggregation, especially prominent when using stealth PFFs invisible to the MJF-14 antibody. Co-labelling of MJF-14 PLA and pS129--synuclein immunofluorescence in post-mortem dementia with Lewy bodies cases showed that while the MJF-14 PLA reveals extensive non-inclusion pathology, it is not sensitive towards Lewy bodies. In Parkinsons disease brain, direct comparison of PLA and IHC with the MJF-14 antibody, combined with machine learning-based quantification, showed striking -synuclein pathology preceding the formation of conventional Lewy pathology. The majority of the PLA-revealed non-inclusion pathology was found in the neuropil, including some clearly located in the presynaptic terminals. With this work, we introduce an improved -synuclein aggregate PLA to uncover abundant non-inclusion pathology, which deserves future validation with multiple brain bank resources and in different synucleinopathies.

neuroscience↗