Publications by authors named "Sachin Tiwari"
Article Synopsis
- Aß pathology primarily influences the expression of Alzheimer's disease risk genes in astrocytes, while both Aß and Tau pathologies trigger age-related changes with some overlapping features found in human AD cases.
- Both Aß and Tau lead to an astrocyte signature that suppresses energy and translation processes, while promoting inflammation and protein degradation, linked to specific mediators like Spi1 and Nrf2.
- Enhancing Nrf2 expression in astrocytes creates a protective reactive phenotype that reduces Aß and Tau accumulation and alleviates neurodegenerative effects and cognitive deficits in mouse models.
Alzheimer's disease (AD) is characterised by Aβ and tau pathology as well as synaptic degeneration, which correlates best with cognitive impairment. Previous work suggested that this pathological complexity may result from changes in mRNA translation. Here, we studied whether mRNA translation and its underlying signalling are altered in an early model of AD, and whether modelling this deficiency in mice causes pathological features with ageing.
View Article and Find Full Text PDFPrion proteins (PrPc) are receptors for amyloid β 1-42 (Aβ1-42) oligomers, but we do not know the impact of Aβ1-42 binding to PrPc on the interaction of membrane-bound PrPc with molecules that regulate downstream biological pathways. Stability of the PrPc dimeric complex and subsequent intermolecular interactions with membranous or cytoplasmic molecules are important for physiological functions of PrPc including neuroprotection. The principal aim of this study was to determine whether homodimer lifetime of PrPc is affected by the presence of Aβ1-42 oligomers.
View Article and Find Full Text PDFArticle Synopsis
- Neurons influence how astrocytes (a type of brain cell) function, but scientists don’t know a lot about it yet.
- Researchers created a special system to study how neurons affect astrocytes and found that certain genes in astrocytes are activated by neurons, which helps astrocytes mature and take up important chemicals.
- They discovered that this process changes as people age and can be affected by brain diseases, showing that neurons and their activity play a big role in how astrocytes work with them to manage energy and communication in the brain.
Characteristic features of Alzheimer's disease are memory loss, plaques resulting from abnormal processing of amyloid precursor protein (APP), and presence of neurofibrillary tangles and dystrophic neurites containing hyperphosphorylated tau. Currently, it is not known what links these abnormalities together. Cytoplasmic FMR1 interacting protein 2 (CYFIP2) has been suggested to regulate mRNA translation at synapses and this may include local synthesis of APP and alpha-calcium/calmodulin-dependent kinase II, a kinase that can phosphorylate tau.
View Article and Find Full Text PDFBackground: In Alzheimer's disease synapse loss precedes neuronal loss and correlates best with impaired memory formation. However, the mechanisms underlying synaptic degeneration in Alzheimer's disease are not well known. Further, it is unclear why synapses in AD cerebellum are protected from degeneration.
View Article and Find Full Text PDFPurpose: To describe the natural course of Type 2 idiopathic macular telangiectasia in terms of visual outcomes, causes of visual loss, and incidence of subretinal neovascular membranes (SRNV).
Methods: This retrospective observational case series consisted of chart review of 104 outpatients (203 eyes; 66 women, 38 men) who were diagnosed to have Type 2 idiopathic macular telangiectasia by clinical examination and fluorescein angiography between January 2000 and December 2008. Visual and anatomic outcomes were analyzed during a minimum follow-up of 1 year.