K S Jagnnathan Rao

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Exposure to high levels of aluminium (Al) leads to neurofibrillary degeneration and that Al concentration is increased in degenerating neurons in Alzheimer's disease (AD). Nevertheless, the role of Al in AD remains controversial and there is little proof directly interlinking Al to AD. The major problem in understanding Al toxicity is the complex Al(More)
Lack of an adequate animal model for Alzheimer's disease (AD) has limited an understanding of the pathogenesis of the disease and the development of therapeutic agents targeting key pathophysiological processes. There are undoubtedly few satisfactory animal models for exploring therapies targeting at amyloid beta (Abeta) secretion, deposition, aggregation,(More)
Amyloid beta (Abeta) deposition and neurodegeneration are the two related events in the pathogenesis of Alzheimer's disease. Several factors modulate the conformation and physical properties of Abeta, which in turn affects its biological functions. Among these, age-dependent changes in the stereospecificity of the amino acids comprising Abeta is one such(More)
alpha-Synuclein filaments are the central component of intracytoplasmic inclusion bodies characteristic of Parkinson's disease (PD) and related disorders. Metals are the significant etiological factors in PD, and their interaction with alpha-synuclein affect dramatically the kinetics of fibrillation. Currently, we have investigated the influence of Cu(II)(More)
Alzheimer's disease (AD) and Parkinson's disease (PD) share several pathological mechanisms. The parallels between amyloid beta (Abeta) in AD and alpha-synuclein in PD have been discussed in several reports. However, studies of the last few years show that Abeta also shares several important characteristics with neuromelanin (NM), whose role in PD is(More)
Amyloid beta (Abeta) is the major etiological factor implicated in Alzheimer's disease (AD). Abeta(42) self-assembles to form oligomers and fibrils via multiple aggregation process. The recent studies aimed to decrease Abeta levels or prevention of Abeta aggregation which are the major targets for therapeutic intervention. Natural products as alternatives(More)
Alzheimer's disease involves Abeta accumulation, oxidative damage and inflammation and there is currently no clinically accepted treatment to stop its progression. Its risk is known to reduce with increased consumption of antioxidant and anti-inflammatory agents. Fibrillar aggregates of Abeta are major constituents of the senile plaques found in the brains(More)
Apoptosis has been implicated in the pathogenesis of various neurodegenerative disorders, although the extent to which it is responsible for the neurodegeneration along with other kind of cell death events is not known. Eventhough much information is available today on the apoptotic cascades in general, the precise mechanism and the exact sequence of events(More)
Alzheimer's disease is the most common form of dementia and is structurally characterized by brain atrophy and loss of brain volume. Aβ is one of the widely accepted causative factors of AD. Aβ deposition is positively correlated with brain atrophy in AD. In the present study, structural brain imaging techniques such as Magnetic Resonance Imaging (MRI) were(More)
Despite the profound burden of Alzheimer's disease (AD) on public health, research to understand its underlying pathology has not yet produced new therapeutic approaches to improve symptoms or halt disease progression. AD is characterized by early cognitive deficits, particularly in short-term memory, followed by a gradual decline in other cognitive(More)