Kiran Yanamandra

ORCID: 0000-0002-4908-5848
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About
Contact & Profiles
Research Areas
  • Alzheimer's disease research and treatments
  • S100 Proteins and Annexins
  • Parkinson's Disease Mechanisms and Treatments
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Prion Diseases and Protein Misfolding
  • Neurological diseases and metabolism
  • Dementia and Cognitive Impairment Research
  • Neurological Disease Mechanisms and Treatments
  • Ocular Surface and Contact Lens
  • Trace Elements in Health
  • Botulinum Toxin and Related Neurological Disorders
  • MicroRNA in disease regulation
  • Nerve injury and regeneration
  • Cell Adhesion Molecules Research
  • Protease and Inhibitor Mechanisms
  • Nuclear Receptors and Signaling
  • Retinal Diseases and Treatments
  • Corneal surgery and disorders
  • Neuroscience and Neuropharmacology Research
  • Ferroptosis and cancer prognosis
  • Advanced Glycation End Products research
  • Extracellular vesicles in disease
  • Neuroscience and Neural Engineering
  • Machine Learning in Bioinformatics
  • Pluripotent Stem Cells Research

AbbVie (United States)
2017-2024

Hope Center for Neurological Disorders
2013-2017

Washington University in St. Louis
2013-2015

Umeå University
2006-2014

Recent experimental evidence suggests that transcellular propagation of fibrillar protein aggregates drives the progression neurodegenerative diseases in a prion-like manner. This phenomenon is now well described cell and animal models involves release into extracellular space. Free then enter neighboring cells to seed further fibrillization. The mechanism by which aggregated proteins such as tau α-synuclein bind trigger intracellular fibril formation unknown. Prior work indicates prion...

10.1073/pnas.1301440110 article EN Proceedings of the National Academy of Sciences 2013-07-29

We previously found a strong reduction in tau pathology and insoluble P301S transgenic mice following intracerebroventricular infusion of the anti-tau antibody HJ8.5. sought to determine effects HJ8.5 same model peripheral administration.The primary objective was if administered at dose 50 mg kg(-1) week(-1) by intraperitoneal (IP) injection 6-month-old for 3 months would influence phospho-tau (p-tau) accumulation, insolubility, neurodegeneration.Treatment with mg/kg showed very decrease...

10.1002/acn3.176 article EN cc-by-nc-nd Annals of Clinical and Translational Neurology 2015-01-23

Auto-antibodies with specificity to self-antigens have been implicated in a wide variety of neurological diseases, including Parkinson's (PD) and Alzheimer's being sensitive indicators neurodegeneration focus for disease prevention. Of particular interest are the studies focused on auto-immune responses amyloidogenic proteins associated diseases their applications therapeutic treatments such as vaccination amyloid antigens antibodies PD, potentially other ailments.Generated auto-antibodies...

10.1371/journal.pone.0018513 article EN cc-by PLoS ONE 2011-04-25

Pathological hallmarks of Alzheimer’s disease (AD) are deposits amyloid beta (Aβ) and hyper-phosphorylated tau aggregates in brain plaques. Recent studies have highlighted the importance Aβ tau-containing extracellular vesicles (EVs) AD. We therefore examined EVs separated from cerebrospinal fluid (CSF) AD, mild cognitive impairment (MCI), control (CTRL) patient samples to profile protein composition CSF EV. EV fractions were AD (n = 13), MCI 10), CTRL 10) using MagCapture Exosome Isolation...

10.3390/cells9091959 article EN cc-by Cells 2020-08-25

Background The conversion of soluble peptides and proteins into polymeric amyloid structures is a hallmark many age-related degenerative disorders, including Alzheimer's disease, type II diabetes variety systemic amyloidoses. We report here that formation linked to another major phenomenon − prostate tissue remodelling in middle-aged elderly men. Methodology/Principal Findings By using multidisciplinary analysis corpora amylacea inclusions glands patients diagnosed with cancer we have...

10.1371/journal.pone.0005562 article EN cc-by PLoS ONE 2009-05-14

Peripheral immune responses can be sensitive indicators of disease pathology. We evaluated the autoimmune reactions to endocrine (insulin) and astrocytical (S100B) biomarkers in blood sera 26 Parkinson's (PD) patients compared with controls by using ELISA. found a statistically significant increase both antigens PD mean 70% 50% towards insulin S100B, respectively. Heterogeneity observed may reflect modulating effect multiple variables associated neurodegeneration also changes basic...

10.1111/j.1468-1331.2006.01667.x article EN European Journal of Neurology 2007-02-06

Abstract Human microglia are critically involved in Alzheimer’s disease (AD) progression, as shown by genetic and molecular studies. However, their role tau pathology progression human brain has not been well described. Here, we characterized 32 donors along of AD pathology, both time—from early to late pathology—and space—from entorhinal cortex (EC), inferior temporal gyrus (ITG), prefrontal (PFC) visual (V2 V1)—with biochemistry, immunohistochemistry, single nuclei-RNA-sequencing,...

10.1007/s00401-024-02704-2 article EN cc-by Acta Neuropathologica 2024-04-01

Objective: Protein aggregation leading to central amyloid deposition is implicated in Parkinson’s disease (PD). During progression, inflammation and oxidative stress may well invoke humoral immunity against pathological aggregates of PD-associated α-synuclein. The aim was investigate any possible concurrence between autoimmune responses α-synuclein monomers, oligomers or fibrils with inflammation. Methods: formation species assessed by thioflavin-T assay atomic force microscopy employed...

10.1159/000341400 article EN NeuroImmunoModulation 2012-01-01

Tau pathobiology has emerged as a key component underlying Alzheimer's disease (AD) progression; however, human neuronal in vitro models have struggled to recapitulate tau phenomena observed vivo. Here, we aimed define the minimal requirements achieve endogenous aggregation functional neurons utilizing induced pluripotent stem cell (hiPSC) technology. Optimized hiPSC-derived cortical seeded with AD brain-derived competent species or recombinant fibrils displayed increases insoluble,...

10.1016/j.isci.2021.103658 article EN cc-by-nc-nd iScience 2021-12-18

Abstract Background In Alzheimer’s disease (AD) progression, amyloid beta load uniformly increases across the brain cortex, while neurofibrillary tangles progressively spread in a stereotypical pattern from entorhinal to visual cortex. AD is known have strong genetic link microglia and recently, expression profiling at single cell resolution has identified disease‐associated populations with differential amyloid‐beta vs. tau pathology association human brain. However, prior studies focusing...

10.1002/alz.062092 article EN Alzheimer s & Dementia 2023-06-01
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