The article reviews the recent findings on the use of optical coherence tomography angiography (OCTA) in neurology. OCTA is a new addition to the powerful and complementary technology of the OCT. Due to its noninvasiveness, and reproducibility, it is possible to obtain high-resolution 3D images of the vessels of the human eye. As the vessels of the retina with the presence of endothelial cell’s tight junctions resemble the brain vessels, it was hypothesized that the imaging of the retinal vessels might bring insight into brain vessels. OCTA has been effectively used to predict retinal vessel abnormalities in dementia, demyelization, optic disc neuropathies, and inherited degenerative diseases. Most common findings were decrease of vascular density and flow and an increase of avascular zones. Although OCTA is a relative new technology, recent studies show that it can be successfully applied in neurology.

/pdf/principles-of-octa-and-applications-in-clinical-neurology-1u01or1m9z.pdf

Principles of OCTA and Applications in Clinical Neurology.

Amyloid-beta peptide neurotoxicity in human neuronal cells is associated with modulation of insulin-like growth factor transport, lysosomal machinery and extracellular matrix receptor interactions.

Optical coherence tomography (OCT) is a non-invasive imaging technique recently used to investigate neurodegenerative disorders, such as Alzheimer’s disease, Parkinson’s disease or multiple sclerosis Over the last years it has been used in schizophrenia research due to the potential utility of its measurements as biomarkers of the disease From the first publication by Ascaso et al (Eur J Psychiat 2010) until now, a number of papers have been published regarding this topic Although the majority of them have found a reduction in the thickness or the volume of some retinal and optic nerve structures, there have also been some results with contradictory data These could be due on the one hand to methodological factors such as the use of different OCT devices or the inclusion/exclusion criteria On the other hand, there could be an important limitation due to the fact that the different stages of the disorder and their different neurobiological correlates and biomarkers were not taken into consideration Future longitudinal studies, that begin the assessments in the first psychotic episode (or even before, in ultra-high risk population) are needed in order to clarify the potential role of some OCT measures as biomarkers in schizophrenia

/pdf/usefulness-of-optical-coherence-tomography-measures-as-4l51sxgx9k.pdf

Usefulness of Optical Coherence Tomography Measures as Biomarkers in Schizophrenia

Increased amyloid β (Aβ) aggregation is a hallmark feature of Alzheimer’s disease (AD) pathology. The APP/PS1 mouse model of AD exhibits accumulation of Aβ in the retina and demonstrates reduced retinal function and other degenerative changes. The overall molecular effects of AD pathology on the retina remain undetermined. Using a proteomics approach, this study assessed the molecular effects of Aβ accumulation and progression of AD pathology on the retina. Retinal tissues from younger (2.5 months) and older 8-month APP/PS1 mice were analysed for protein expression changes. A multiplexed proteomics approach using chemical isobaric tandem mass tags was applied followed by functional and protein-protein interaction analyses using Ingenuity pathway (IPA) and STRING computational tools. We identified approximately 2000 proteins each in the younger (upregulated 50; downregulated 36) and older set of APP/PS1 (upregulated 85; downregulated 79) mice retinas. Amyloid precursor protein (APP) was consistently upregulated two to threefold in both younger and older retinas (p < 0.0001). Mass spectrometry data further revealed that older APP/PS1 mice retinas had elevated levels of proteolytic enzymes cathepsin D, presenilin 2 and nicastrin that are associated with APP processing. Increased levels of proteasomal proteins Psma5, Psmd3 and Psmb2 were also observed in the older AD retinas. In contrast to the younger animals, significant downregulation of protein synthesis and elongation associated proteins such as Eef1a1, Rpl35a, Mrpl2 and Eef1e1 (p < 0.04) was identified in the older mice retinas. This study reports for the first time that not only old but also young APP/PS1 animals demonstrate increased amyloid protein levels in their retinas. Quantitative proteomics reveals new molecular insights which may represent a cellular response to clear amyloid build-up. Further, downregulation of ribosomal proteins involved in protein biosynthesis was observed which might be considered a toxicity effect.

Upregulation of Proteolytic Pathways and Altered Protein Biosynthesis Underlie Retinal Pathology in a Mouse Model of Alzheimer's Disease.

Page 11 of 13 Retinal changes in Alzheimer’s disease: Disease Mechanisms to Evaluation perspectives M Mirzaei1,2,3*, VB Gupta4, VK Gupta2 1Department of Molecular Sciences, Macquarie University, Sydney, NSW, Australia 2Department of Clinical Medicine, Macquarie University, Sydney, NSW, Australia 3Australian Proteome Analysis Facility, Macquarie University, Sydney, NSW, Australia 4School of Medical Sciences, Edith Cowan University, Joondalup, WA, Australia

/pdf/retinal-changes-in-alzheimer-s-disease-disease-mechanisms-to-3ws7jjqud3.pdf

Retinal changes in Alzheimer's disease: Disease Mechanisms to Evaluation perspectives.

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Retinal changes in Alzheimer's disease: Disease Mechanisms to Evaluation perspectives.