Publications by authors named "Ashini Singh"

Article Synopsis
  • - PDE5 is an enzyme that breaks down cGMP, a molecule crucial for enhancing neural signals and influencing learning and memory processes, and it's found in the brain and in the smooth muscle of the corpus cavernosum.
  • - PDE5 inhibitors, which prevent the breakdown of cGMP, can enhance nitric oxide effects, providing anti-inflammatory and neuroprotective benefits, potentially addressing neurodegenerative disorders, which currently lack curative treatments.
  • - The review explores how PDE5 inhibitors may act as disease-modifying agents for conditions like Alzheimer's and Parkinson's diseases by simultaneously influencing both cAMP and cGMP pathways, potentially improving neurological functions.
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Parkinson's disease (PD) stands as the second most common neurological disorder after Alzheimer's disease, primarily affecting the elderly population and significantly compromising their quality of life. The precise etiology of PD remains elusive, but recent research has shed light on potential factors, including the formation of α-synuclein aggregates, oxidative stress, neurotransmitter imbalances, and dopaminergic neurodegeneration in the substantia nigra pars compacta (SNpc) region of the brain, culminating in motor symptoms such as bradykinesia, akinesia, tremors, and rigidity. Monoamine oxidase (MAO) is an essential enzyme, comprising two isoforms, MAO-A and MAO-B, responsible for the oxidation of monoamines such as dopamine.

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Parkinson's disease (PD), the most common brain-related neurodegenerative disorder, is comprised of several pathophysiological mechanisms, such as mitochondrial dysfunction, neuroinflammation, aggregation of misfolded alpha-synuclein, and synaptic loss in the substantia nigra pars compacta region of the midbrain. Misfolded alpha-synuclein, originating from damaged neurons, triggers a series of signaling pathways in both glial and neuronal cells. Activation of such events results in the production and expression of several proinflammatory cytokines via the activation of the nuclear factor κB (NF-κB) signaling pathway.

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Neurodegenerative disorders (NDs) are a group of progressive, chronic, and disabling disorders that are highly prevalent and the incidence is on a constant rise globally. Alzheimer's disease (AD), one of the most common neurodegenerative disorders is hallmarked by cognitive impairment, amyloid-β (Aβ) deposition, hyperphosphorylation of tau protein, cholinergic dysfunction, mitochondrial toxicity, and neurodegeneration. Available therapeutic agents only provide symptomatic relief and their use are limited due to serious side effects.

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Parkinson's disease (PD) is the second most prevalent neurodegenerative disorder, and its consequences severely influence the quality of a patient's life and mobility. PD is characterized by bradykinesias with tremors and/or rigidity. Pathophysiologically, PD is associated with the gradual degeneration of dopaminergic neurons in the substantia nigra pars compacta of the midbrain, neuroinflammation, increased accumulation of the alpha (α)-synuclein, overburden of oxidative stress, and mitochondrial dysfunction.

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Synopsis of recent research by authors named "Ashini Singh"

  • - Ashini Singh's research primarily focuses on neurodegenerative disorders, particularly Parkinson's disease and Alzheimer's disease, exploring both the molecular mechanisms involved and potential therapeutic interventions.
  • - Recent studies highlighted include the role of phosphodiesterase 5 inhibitors in enhancing cGMP signaling for neuroprotection, the protective effects of dietary flavonoids against MAO-B related neurotoxicity, and the significance of NF-κB as a therapeutic target in neuroinflammation and neuronal degeneration.
  • - Singh's work emphasizes natural compounds like naringin and exendin-4, showcasing their neuroprotective potentials, which could offer alternative approaches to conventional therapies with extensive side effects in treating debilitating conditions like Alzheimer's and Parkinson's diseases.