Publications by authors named "Veer Bala Gupta"

Article Synopsis
  • * Emerging research highlights mitochondrial dysfunction and protein aggregation as common factors in these disorders, while innovative therapies, such as gene therapy and antioxidants, are being explored to manage these conditions.
  • * Lifestyle changes like exercise and a healthy diet show potential in improving brain health, and advancements in neuroimaging and biomarker discovery are crucial for early diagnosis and effective treatment strategies.
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  • * Using gene therapy techniques, researchers found that both increasing and decreasing Tau levels negatively affected the health and function of retinal neurons.
  • * The results suggest that higher Tau levels can worsen retinal degeneration in glaucoma, while reducing Tau levels may offer protective benefits, highlighting Tau as a potential therapeutic target for the disease.
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Background: Poor cognitive function, a major disabling condition of older age, is often considered a prodromal feature of dementia. High mortality and the lack of a cure for dementia have necessitated a focus on the identification of potentially modifiable risk factors. Mental and physical health conditions such as mood disorders and bone loss have been previously linked with poor cognition individually although their combined effect remains largely unknown.

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  • Lip, oral, and pharyngeal cancers pose significant global health challenges, making it essential to analyze their burden for effective health policies.
  • The study utilized data from the 2019 Global Burden of Diseases, Injuries, and Risk Factors Study to assess cancer incidence, mortality, and life years lost across 204 countries, linking these to socio-demographic factors.
  • Findings revealed approximately 370,000 cases and 199,000 deaths for lip and oral cavity cancer, and 167,000 cases and 114,000 deaths for other pharyngeal cancers in 2019, with smoking being the leading risk factor for these cancers, especially in low and middle SDI regions.
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Background: A minimally invasive blood-based assessment of cognitive function could be a promising screening strategy to identify high-risk groups for the incidence of Alzheimer's disease.

Methods: The study included 448 cognitively unimpaired men (mean age 64.1 years) drawn from the Geelong Osteoporosis Study.

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Although several genetic polymorphisms have been linked with the risk of Alzheimer's disease, less is known about their impact on cognitive performance among cognitively healthy individuals. Our aim was to investigate the association of the genetic variant, rs744373 in the bridging integrator 1 gene (BIN1), the strongest genetic risk factor for Alzheimer's disease after the APOE ε4 allele, with different cognitive domains among non-demented older men. Cognitive function was measured using the CogState Brief Battery, which assessed cognitive performance across four domains: psychomotor function, visual attention, recognition memory and working memory.

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Background: Depression is linked to Alzheimer's disease (AD) but it is unclear whether depression is also associated with cognitive decline in the preclinical phase and mild cognitive impairment (MCI). Previous meta-analyses have only investigated AD as an outcome without accounting for individuals showing cognitive decline that does not meet the diagnostic criteria for AD. Other potentially modifiable risk factors such as bone loss have also been less explored and there remains uncertainty around their temporal relationship with cognitive decline.

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  • The GBD 2019 study systematically estimated the global cancer burden, providing data on incidence, mortality, and disability to help address cancer worldwide.
  • In 2019, an estimated 23.6 million new cancer cases and 10 million cancer deaths occurred globally, marking significant increases in rates since 2010, with cancer becoming a leading cause of both death and disability-adjusted life years (DALYs).
  • The impact of cancer varied across sociodemographic index (SDI) quintiles, with higher SDI areas seeing more new cases, while middle SDI areas experienced more deaths and DALYs, highlighting disparities in cancer burden.
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  • In 2008, guidelines were established for researching autophagy, which has since gained significant interest and new technologies, necessitating regular updates to monitoring methods across various organisms.
  • The new guidelines emphasize selecting appropriate techniques to evaluate autophagy while noting that no single method suits all situations; thus, a combination of methods is encouraged.
  • The document highlights that key proteins involved in autophagy also impact other cellular processes, suggesting genetic studies should focus on multiple autophagy-related genes to fully understand these pathways.
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Multifactorial pathological processes of Alzheimer's disease (AD) begin decades prior to clinical onset. Early identification of patients at risk of developing AD using biomarkers reflecting various aspects of pathogenesis is necessary for prevention and early intervention. Cortical β-amyloid (Aβ) burden assessed by positron emission tomography (PET) or cerebrospinal fluid (CSF) levels of Aβ42 are validated biomarkers for early identification.

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Introduction: This study assessed the utility of cerebrospinal fluid (CSF) neurofilament light (NfL) in Alzheimer's disease (AD) diagnosis, its association with amyloid and tau pathology, as well as its potential to predict brain atrophy, cognition, and amyloid accumulation.

Methods: CSF NfL concentration was measured in 221 participants from the Australian Imaging, Biomarkers & Lifestyle Flagship Study of Ageing (AIBL).

Results: CSF NfL levels as well as NfL/amyloid β (Aβ42) were significantly elevated in AD compared to healthy controls (HC; < .

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Alzheimer's disease (AD) is a multifactorial age-related brain disease. Numerous pathological events run forth in the brain leading to AD. There is an initial long, dormant phase before the clinical symptoms become evident.

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Accumulating evidence suggests a diet high in protein and fiber may confer some protection against Alzheimer's disease (AD). However, no human studies to-date have assessed the relationship between protein and fiber intake, and plasma and brain amyloid-β (Aβ). Consequently, this cross-sectional study, investigated the association of self-reported dietary intakes of protein and fiber, with plasma and brain Aβ burden (n = 541, and n = 162 respectively), in a well-characterized cohort of cognitively normal older adults, drawn from the larger Australian Imaging, Biomarkers and Lifestyle (AIBL) study of aging.

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Neuroserpin is a serine protease inhibitor that regulates the activity of plasmin and its activators in the neuronal tissues. This study provides novel evidence of regulatory effect of the neuroserpin on plasmin proteolytic activity in the retina in glaucoma. Human retinal and vitreous tissues from control and glaucoma subjects as well as retinas from experimental glaucoma rats were analysed to establish changes in plasmin and neuroserpin activity.

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Alzheimer's disease (AD) is progressive neurodegenerative disorder characterized by accumulation of senile plaques, neurofibrillary tangles (NFT) and neurodegeneration. The diabetes mellitus (DM) is one of the risk factors for AD pathogenesis by impairment in insulin signaling and glucose metabolism in central as well as peripheral system. Insulin resistance, impaired glucose and lipid metabolism are leading to the Aβ (Aβ) aggregation, Tau phosphorylation, mitochondrial dysfunction, oxidative stress, protein misfolding, memory impairment and also mark over Aβ transport through central to peripheral and vice versa.

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Introduction: A blood-based biomarker panel to identify individuals with preclinical Alzheimer's disease (AD) would be an inexpensive and accessible first step for routine testing.

Methods: We analyzed 14 biomarkers that have previously been linked to AD in the Australian Imaging Biomarkers lifestyle longitudinal study of aging cohort.

Results: Levels of apolipoprotein J (apoJ) were higher in AD individuals compared with healthy controls at baseline and 18 months ( = .

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Introduction: For early detection of Alzheimer's disease (AD), the field needs biomarkers that can be used to detect disease status with high sensitivity and specificity. Apolipoprotein J (ApoJ, also known as clusterin) has long been associated with AD pathogenesis through various pathways. The aim of this study was to investigate the potential of plasma apoJ as a blood biomarker for AD.

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Advances in the field of blood biomarker discovery will help in identifying Alzheimer's disease in its preclinical stage, allowing treatment to be initiated before irreversible damage occurs. This review discusses some recent past and current approaches being taken by researchers in the field. Individual blood biomarkers have been unsuccessful in defining the disease pathology, progression and thus diagnosis.

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The Trk family of receptors play a wide variety of roles in physiological and disease processes in both neuronal and non-neuronal tissues. Amongst these the TrkB receptor in particular has attracted major attention due to its critical role in signalling for brain derived neurotrophic factor (BDNF), neurotrophin-3 (NT3) and neurotrophin-4 (NT4). TrkB signalling is indispensable for the survival, development and synaptic plasticity of several subtypes of neurons in the nervous system.

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Background: Mexican Americans are the fastest aging segment of the U.S. population, yet little scientific literature exists regarding the Alzheimer's disease (AD) among this segment of the population.

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Alzheimer's disease is characterized pathologically by the deposition of amyloid plaques. Fibrillar Abeta is the principal component of amyloid plaques in the brain of AD patients. The prevention of Abeta aggregation or dissolution of fibrillar Abeta has clinical significance.

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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 factors.

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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 of AD patients and have been related to AD neurotoxicity.

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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 leading to neuronal degeneration in Alzheimer's disease (AD) and other neurodegenerative disorders is not understood till now. Amyloid beta (Abeta) proteins are the hallmark toxic proteins known to cause the activation of apoptotic cascades via caspase dependent and caspase-independent pathways.

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