NUST Institutions Library Catalogue Search for 'kw,wrdl: su-br:an:"11951"'

Role of Nucleobindin 1 in Clozapine-Induced Neuroprotection in MPTP-Treated Mice Models /

By Bhatti, Rohama Makmas . . 64p. 30cm.

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Characterization of the Role of Neurexin-1 in MPTP Induced Parkinsonism in Mice Model /

By Naeem, Mahnoor . . 62p. 30cm.

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Effects of Cassia Angustifolia and Nigella Sativa for the prevention of Diabetic Neuropathy /

By Khan, Mahum. . 81p. 30cm.

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Therapeutic Potential of Rutin-Bound Glucose Carbon Dots for Alzheimer’s Disease /

By Khan, Sana. . 76p. 30cm.

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Early Diagnosis of AD by Detecting Amyloid-Beta in the Retina of AD-Induced Mice Using IR Spectroscopy /

By Waheed, Zuha. . 66p. 30cm.

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Identification and Characterization of Hormonal Response in Depression Induced Mice Models /

By Ilyas, Noor-Ul-Ain. . 55p. , Background: Early life stress is correlated with escalated peril for anxiety, mood, substance, impulse control and depressive disorders. Such disorders might spring from chemical imbalance in brain. A well-grounded mouse prototype of childhood adversity contributing to the everlasting behavioral changes in an individual would help understand the mechanism underlying these adverse effects. Maternal deprivation is frequently used paradigm of early neglect. Natriuretic peptides especially Atrial Natriuretic Peptide (ANP) released from Atrial myocytes have significant anxiolytic role corroborated by certain animal and human trails. The concentration of ANP has been found to be elevated by Levothyroxine (LT4) which treats the adverse symptoms of anxiety and depression. Method and Results: In an attempt to contrive the paradigm of childhood adversity in mouse models with everlasting impacts on behavior of balb/c mice, maternal separation model followed by early weaning model were developed and behavioral tests were performed 60 days following maternal separation followed by early weaning (MSEW) paradigm for the validation of model. The experimental and control groups were further divided into 3 groups: MSEW group with drug administration, MSEW group with no drug administration and control group with no MSEW and no drug administration. Following a 7 days administration of LT4 at the concentration of 15 micrograms per mice to MSEW group and one of the control groups, decline in anxiety level in mice subjected to MSEW was observed in comparison to the MSEW group that was not administered LT4. These findings were validated by performing anxiety related paradigms after drug injection and the difference in the behavior was observed accordingly which suggested decrease in behavioral despair and anxiety related symptoms in mice. Conclusion: Our findings elucidate that maternal separation model followed by early weaning contributes as a substantial paradigm to scrutinize the intricate behavioral anomalies in organisms with early life adversity history and by increasing the concentration of ANP by injection of LT4 cures the anxiety-related symptoms and provides a n apprehension for a futuristic therapeutic plan of actions. 30cm.

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Characterization of atrial natriuretic peptide (ANP) response in depression-induced mice models /

By Ali, Saman . . 71p. , Depression is a complex psychological disorder that is also often link to the hormonal imbalances. Our research delves into the intricate relationship between depression and atrial Natriuretic Peptide (ANP), considering the multifaceted influences of neurological, genetic, and environmental factors. With a focus on hormonal imbalances as key contributors to depression, our investigation explores the potential therapeutic effects of Levothyroxine (LT4) in the context of ANP. Utilizing an early weaning mouse model involving maternal separation, we conducted a detailed examination of the anxiolytic effects of LT4, aiming to evaluate its efficacy in alleviating symptoms associated with anxiety and depression. Behavioral assessments and histological analyses were employed to comprehensively evaluate the impact of LT4 on ANP. This study also extends to molecular investigations using RT-PCR to analyze the distribution and expression of ANP within the mouse central nervous system, highlighting the cortex region. Our findings reveal significant differences in brain expression levels of ANP between treated mice and those exhibiting depressive symptoms. This insight suggests potential therapeutic applications of ANP for mitigating depression, presenting intriguing avenues for further research, particularly in the context of depression-induced mouse models through parental separation. This research contributes to an enriched understanding of the complex factors influencing depression and proposes interventions that extend beyond conventional approaches. The integration of behavioral assessments, histological analyses, and molecular investigations offers a holistic perspective, laying the groundwork for future exploration in the critical realm of mental health research. 30cm.

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Therapeutic Potential of Galantamine for Managing the Complications Associated with Ischemic Stroke /

By Ahsan, Mehwish . . 104p. , Ischemic stroke remains the leading cause of illness and second leading cause of death worldwide. Previous research has shown that galantamine has neuroprotective properties, reducing neuronal death and damage in neurodegenerative conditions and improving cognitive function in Alzheimer's disease patients. The investigation looked into the possible mechanisms by which this medication could reduce cell death. Wistar rats were subjected to a temporary 30-minute occlusion of the right middle cerebral artery (MCA) and given an oral dose of 5mg/kg for three weeks. After 18 days of surgery, behavioral assessments were carried out. Galantamine enhanced grip strength, motor function, and muscle strength in rats. Spatial memory and object recognition examinations revealed cognitive improvements, thus indicating enhanced cognitive abilities and memory retention. Moreover, rats subjected to galantamine treatment displayed increased sociability and heightened locomotor activity during social interaction and open-field assessments. Molecular analysis of galantamine treatment in rats showed an upregulation of SOD2 expression, suggesting enhanced antioxidant defense, and a downregulation of TLR4 expression, suggesting a reduction in neuroinflammation, supporting the anti-inflammatory properties of galantamine. The histological analysis done with H&E staining of brain tissue revealed enhanced tissue morphology in the galantamine-treated group, signifying the neuroprotective effects of galantamine. The reduction in neuronal damage, edema, and inflammatory cell infiltration further supported this observation. The results demonstrate that galantamine, potentially through the preservation of a functional cholinergic system, mitigated the impairments caused by stroke in a basic learning and memory test by decreasing cellular death. 30cm.

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Effectivity of Rutin-bound Carbon dots in preventing the aggregation of Amyloid beta /

By Noor Afza. . 78p. , According to the World Health Organization up to 55 million people have dementia resulting in concerning socio-economic implications. About 60-80% cases of dementia are associated with Alzheimer's disease. With all the advances in medicine, there still is no cure. Blood-brain barrier monitors the entry and exit of nutrients and molecules which makes it difficult for various drugs and therapeutic molecules to cross it. Carbon dots are made from glucose to overcome the BBB. Rutin is a naturally existing flavonoid extracted from plants and has therapeutic effects in neuroprotection. This study aims to improve the effectiveness of rutin combined with targeted delivery of carbon dots. Carbon dots were loaded with Rutin to make CD-Rutin, a nano-sized combination with a targeted drug. FTIR, UV-IR, and SEM analysis have produced positive results regarding the doping of CDs with Rutin. Administration of CD-Rutin was done in AD-like rat models at eight to twelve months of age. Alzheimer's was induced in rats with Aluminum Chloride and D-galactose through IP administration for two weeks. Behavioral tests were performed to check the progression of the disease. In silico analysis was also done to check ligand-protein interaction to check variation in the binding of Aβ isoforms with Rutin. Afterward, a single injection of CD-Rutin (10 mg/kg) was given intraperitoneally as well. Behavioral testing was done after the administration of the drug. Characterization techniques revealed the successful formation of CDs and subsequent loading of Rutin onto the CDs resulting in a CD-Rutin combination. In silico analysis provided strong binding affinities of Rutin with Aβ isoforms affirming Rutin as a favorable treatment to target amyloid aggregates. 3D configuration showed binding of Rutin with hydrophobic domains of protein oligomers Behavioral testing provided significant difference in the treated group with better memory retention and performance in activities involved in behavioral testing. After behavioral testing, rats were dissected for molecular analysis including H&E to assess cell degeneration and Thioflavin T staining to assess amyloid aggregates in the brain tissues. Results provided positive data in terms of cell count in the cortex. Overall results suggest that memory impairment and cognitive abilities were significantly improved after injections. The results demonstrate the positive therapeutic potential of CD-Rutin in Alzheimer's treatment. 30cm.

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Therapeutic Potential of Rivastigmine for Managing Complications Associated with Ischemic Stroke /

By Abbasi, Irum Naeem . . 80p. , Stroke continues to be the world’s primary cause of morbidity and mortality, frequently with incapacitating consequences like movement dysfunction, cognitive decline, and neurological impairments. It is essential to manage stroke effectively to lessen its negative effects and enhance patient outcomes. The potential neuroprotective benefits of acetylcholinesterase inhibitors may assist maintain the integrity of brain tissue and lessen the damage that neurons may sustain after a stroke, making them a promising option in this situation. This comprehensive thesis explores the neuroprotective benefits of an acetylcholinesterase inhibitor, Rivastigmine, in relation to stroke outcomes in a variety of ways. Using an advanced integrative methodology, this study includes behavioral evaluations, in silico analysis, histopathological results, and molecular studies to give a comprehensive picture of the possible mechanisms behind therapeutic effects of Rivastigmine. Within the field of computer modelling, the docking interactions between SOD2 and TLR4, the target proteins of Rivastigmine, provide detailed structural information that directs further experimental validations. Following Rivastigmine treatment, the behavioral tests conducted exhibited improvements in cognitive, motor, and social domains. These results were further corroborated by histopathological analysis, which shows neuroprotective effects in Rivastigmine treated group as opposed to surgery (MCAO) group. Post Rivastigmine treatment, real-time PCR data showed a rise in SOD2 and a decrease in TLR4 levels in surgery (MCAO) rats, exhibiting antioxidant and anti-inflammatory effects of Rivastigmine. These findings provide interesting directions for future neuroprotective approaches and shed light on the possible therapeutic implications of Rivastigmine in reducing neurodegeneration that occurs in stroke. 30cm.

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Investigating Chrysoeriol-Mediated Protection in MPTP-Induced Mouse Model of Parkinson's Disease /

By Ali ,Mehak. . 105p. ; , Parkinson's disease (PD) is a neurodegenerative condition characterized by the progressive loss of dopamine-producing neurons in the substantia nigra pars compacta, which results in severe motor impairments. While the precise cause of PD remains unknown, research indicates that factors such as oxidative stress, mitochondrial dysfunction, and the triggering of apoptotic pathways play key roles in the degeneration of these neurons. Current treatments focus on stabilizing dopamine levels but do not halt disease progression. Therefore, exploring compounds that can mitigate apoptotic neuronal loss is promising for therapy. Chrysoeriol, a 3’-O-methoxy flavone and luteolin derivative, is known for its anti-cancer, anti-diabetic, antioxidant, anti-inflammatory, and neuroprotective properties. Despite extensive research, its effect on PD mouse models is still unclear. This study examines the neuroprotective effects of 5 mg/kg of Chrysoeriol administered intraperitoneally for 14 days in an in vivo sub-acute PD model, established using 20 mg/kg MPTP administered via intraperitoneal injections at two-hour intervals for a total of four doses in one day. Behavioral tests, including the Pole test, Y-maze test, forced swim test, and tail suspension test, showed significant recovery from PD-induced neurological deficits in Chrysoeriol-treated mice. Hematoxylin and Eosin staining confirmed reduced neuronal damage in Chrysoeriol-treated mice in different areas of the brain, including the midbrain, cerebellum, cortex, and hippocampus. qPCR analysis was used to detect the relative expression of α-Synuclein, Bcl-2 (anti-apoptotic) and Bax (pro-apoptotic) proteins. The levels of α-synuclein, a major protein implicated in PD pathology, were significantly downregulated in the treatment group compared to the diseased group, indicating that Chrysoeriol plays a role in the downregulation of α-synuclein. Moreover, in the diseased group, Bax levels were up-regulated, and Bcl-2 levels were downregulated, reducing the Bcl-2/Bax ratio. Chrysoeriol treatment significantly reversed this downregulation. Our results demonstrated that Chrysoeriol treatment significantly reduced MPP+- induced toxicity, downregulated α-synuclein expression levels, and improved Bcl-2/Bax ratio expression levels in in vivo mouse models. Our research indicates that Chrysoeriol offers protection against MPP+-induced apoptosis in mice by activating the PI3K/Akt signaling pathway. This finding suggests that Chrysoeriol could be a promising therapeutic option for PD. 30cm..

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Investigating the Neuroprotective Effects of Chenodeoxycholic Acid in MPTP-induced Parkinson’s disease in BALB/c mice /

By Mehreen ,Mehwish. . 77p. ; , Parkinson's disease (PD) remains a major challenge in the field of neurodegenerative diseases and requires innovative therapeutic approaches. In this study, we investigated the therapeutic potential of chenodeoxycholic acid (CDCA) in PD using a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced mouse model. CDCA, a naturally occurring bile acid, has previously shown promise in various neurological disorders by reducing neuronal degeneration and promoting neuronal health, however its utility in PD has not been studied. Mice were divided into a control group, an MPTP-induced PD model (20 mg/kg, intraperitoneally) and a treatment group injected intraperitoneally with CDCA (90 mg/kg). CDCA reduced motor impairment and ameliorated anxiety-like behavior as assessed by the pole test and open field test, demonstrated antidepressant effects in the forced swim test and tail suspension test, and results of the Y-maze test showed improved cognitive performance. Furthermore, the effective defense against MPTP-induced dopaminergic degeneration was provided by CDCA through improving the morphological and histological features of neurons in the midbrain, hippocampus, cortex and cerebellum. Additionally, the biomarkers used in this study are brain-derived neurotrophic factor (BDNF) and α-synuclein. Hence, treatment with CDCA significantly mitigated MPTP-induced elevations in α- synuclein levels, indicating that it may have potential to preserve and recover neuronal function. Moreover, the neurotrophic role of CDCA was demonstrated by improving the low levels of BDNF in the presence of MPTP. The results of this study promise valuable insights into the potential therapeutic properties of CDCA in reducing the effects of PD and provide a basis for further research into bile acid-based treatments in neurodegenerative diseases. 30cm..

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Proteomic Analysis of Alzheimer’s Disease Models Administered with Rutin and Rutin-Bound Nanoparticles /

By Muti ,Alveena. . 86p. ; , Alzheimer’s disease is a progressive neurodegenerative disease leading to cognitive impairment and memory loss. The presence of amyloid ß deposition and neurofibrillary tangles remain the neuropathologic criteria for AD diagnosis. The BBB which is necessary for proper neuronal activity prevents solutes from the bloodstream getting into the brain. Unfortunately, there is no effective therapy for the treatment of AD due to low drug potency and various drug delivery issues, such as limited bioavailability and the blood-brain barrier's obstructions. Recently nanotechnology has demonstrated encouraging advancements in the treatment of AD. Many different types of nano-carriers have been modified to provide effective new therapeutic approaches. This study investigated therapeutic effect of Rutin and compared them with those of Rutin-bound nanoparticles, NCDs-Rutin and CDs-Rutin in AD rat model. AD was induced in Wistar Han rats using AlCl3 and D-galactose. The rats were then treated with Rutin and Rutin-bound nanoparticles and the effects were assessed using different parameters. Behavior assessment showed that NCDs-Rutin gave significant results in MWM, Y-maze and NOR test, while CDs-Rutin exhibited better result in open field test. Histological analysis using H & E staining revealed that NCDs-Rutin group prevented brain tissue better than CDs-Rutin and Rutin group, however, Rutin group had more effective amyloid plaque reduction in ThT staining. Moreover, molecular analysis of treatment groups showed an upregulation of SOD2 expression, among them NCDs-Rutin and Rutin group showed significant results suggesting enhanced antioxidant defense. While, CDs-Rutin group showed significant reduction in TLR4 expression, suggesting a reduced neuroinflammation. Proteomic analysis through SDS-PAGE indicated differences protein expression across the groups. The Rutin-bound nanoparticles significantly outperformed Rutin in terms of efficacy, most likely as a result of their focused administration and increased bioavailability. 30cm..

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Investigating the Neuroprotective Impacts of Chenodeoxycholic Acid in STZ-Induced Diabetic Neuropathy and Cognitive Impairment in BALB/c Mice /

By Bano, Maria . . 77p. , Diabetic neuropathy and cognitive impairment are common complications of diabetes, significantly affecting the lives of millions of people. Finding effective treatments for these issues remains a critical challenge. In this study, we investigated whether chenodeoxycholic acid, a naturally occurring bile acid known for its neuroprotective properties, could help alleviate these complications. We utilized a mouse model of diabetes induced by streptozotocin. The mice were categorized into three groups; a healthy control, a diabetic group and a diabetic group that receive treatment with CDCA. The diabetic mice displayed typical signs of nerve pain, anxiety-like behaviour, and memory problems. However, those treated with CDCA showed remarkable improvements in all these areas. They experienced less pain in the hot plate analgesia, exhibited reduced anxiety levels in the open field test, and demonstrated better memory and cognitive function in the test of Y-maze. Beyond behaviour, CDCA also had profound effects on the brain. It preserves the structure of neurons in critical areas like the hippocampus and cortex, which are often affected by diabetic neuropathy. At a molecular level, CDCA may reduce inflammation by decreasing nuclear factor kappa B levels, a key marker of inflammation and cell damage. The brain-derived neurotrophic factor is also increased, a protein essential for nerve growth and repair in the brain, suggesting that CDCA supports the brain’s natural ability to heal. These results provide a promising glimpse into the potential of CDCA as a treatment for diabetes-related nerve and cognitive problems. While more research is needed, the ability of CDCA to protect neurons, reduce inflammation, and improve cognitive and behavioural outcomes makes it a promising drug for future therapies aimed at improving the lives of people with diabetes. 30cm.

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Therapeutic Potential of Light Flicker for Schizophrenia - A Comparative Study

By Ihsan ,Faryal. . 93p. ; , Schizophrenia is a serious neuropsychiatric condition that affects cognition, perception, and behavior. Current pharmacological treatments are successful in treating symptoms but can have serious adverse effects, especially in susceptible populations such as children and the elderly. These negative consequences, which range from metabolic problems to cognitive impairment, underline the critical need for alternate, non-invasive therapeutic techniques. One promising approach is neuromodulation by gamma entrainment with sensory stimulation, which uses an external stimulus to restore broken neuronal synchronization. This study looks at the combined effects of Clozapine and light flicker therapy in a ketamine-induced schizophrenia mouse model, with the hypothesis that their synergistic action will lead to improved recovery. Mice were classified into five groups: control, diseased, Clozapine-treated, light flicker-treated, and combination therapy. Behavioral examinations, such as the open field test, elevated plus maze, forced swim test, tail suspension test, novel object recognition, and Y-maze, demonstrated that combination therapy improved cognitive and affective deficiencies the most significantly. Histological analysis with hematoxylin and eosin staining of the cortex and hippocampus (CA1 and CA3) revealed severe neuronal disorganization in the diseased group, partial restoration in the individual treatment groups, and near-control level preservation in the combination therapy group. RT-PCR analysis using Pvalb and BDNF primers indicated abnormalities in PV interneurons and neuroplasticity markers, which corroborated the histological and behavioral findings. Our approach to schizophrenia combines neuroscience and psychology. Restoring gamma oscillations with light flicker improves PV interneuron function, BDNF production, and cognitive stability. This neuronal synchronization minimizes ego fragmentation, improves self perception, and promotes cognitive integration for a more comprehensive treatment. 30cm..

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Therapeutic Effects of Light Flicker Stimulation in a Mouse Model of Depression - A Comparative Study /

By Hyder, Azan . . 80p. , Depression is a common neuropsychiatric condition, characterized by behavioral deficiencies, mood swings, and cognitive impairments. Although fluoxetine is still a commonly prescribed antidepressant, its drawbacks, including systemic side effects and delayed therapeutic results, make it necessary to look at alternative treatments. Using a chronic restraint stress mouse model, this study examines the effectiveness of 40 Hz light flicker therapy as a novel, non-invasive neuromodulatory treatment for depression by directly contrasting it with fluoxetine treatment. Behavioral tests such as the Light-Dark Box, Forced Swim, and Sucrose Preference tests showed that 40 Hz light stimulation dramatically reduced depressive-like behaviors, frequently outperforming the effects of fluoxetine. Histopathological examinations showed that parvalbuminexpressing interneurons, which are necessary for gamma oscillatory activity and inhibitory circuitry, had been protected in the prefrontal cortex (PFC) and hippocampal regions. Increased expression of brain-derived neurotrophic factor (BDNF) and parvalbumin (PV) was further validated by molecular experiments, suggesting improved interneuron integrity and neuroplasticity. These results demonstrate that 40 Hz light flicker therapy facilitates the functional restoration of brain regions damaged in depression, pointing to distinct mechanisms from those of traditional medication. Subsequent research endeavors ought to concentrate on refining stimulation parameters, evaluating long-term safety and effectiveness, and clarifying electrophysiological mechanisms via supplementary imaging and neurophysiological studies. Promising translational potential is indicated by ongoing clinical investigations. To conclude, 40 Hz light flicker therapy might prove to be a useful supplement or substitute therapy, providing a customized, side-effect-free choice for managing depression. 30cm.

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Therapeutic Effects of Sound-Mediated Stimulation in a Mouse Model of Depression - A Comparative Study /

By Reemaz, Tooba . . 90p. , Depression is a prevalent neuropsychiatric disorder characterized by mood disturbances, cognitive impairment, and behavioral deficits. While pharmacological treatments such as Fluoxetine are widely used, they often represent limitations including delayed onset of action and side effects, highlighting the need for alternative, non-invasive therapeutic strategies. One promising approach is neuromodulation through gamma entrainment using auditory stimulation, aimed at restoring disrupted neuronal synchronization. This study evaluates the effects of 40 Hz sound stimulation compared to fluoxetine in a chronic restraint stress-induced mouse model of depression, hypothesizing that sound therapy will yield superior recovery outcomes. Mice were divided into control, depressed, fluoxetine-treated, and sound stimulation-treated groups. Behavioral assessments, including the Tail Suspension Test, Forced Swim Test, Social Interaction Test, Sucrose Preference Test, Open Field Test, and Light-Dark Box Test, revealed that 40 Hz sound therapy significantly alleviated depressive-like behaviors, often outperforming fluoxetine. Histopathological analysis focused on the hippocampus and prefrontal cortex showed that sound stimulation preventing neuronal loss and parvalbumin-expressing interneurons, which are crucial for inhibitory circuit function and gamma oscillatory activity. Molecular evaluation through qPCR for pavlb and brain-derived neurotrophic factor; BDNF supported these findings, displaying increased expression levels indicating enhanced interneuron integrity and neuroplasticity. This neuromodulatory treatment encourages the molecular and functional repair of brain circuitry implicated in depression. The findings demonstrated 40 Hz sound entrainment's ability to change brain oscillations and ameliorate cellular and behavioral deficiencies linked to depression, indicating that it may be a novel supplement or substitute for traditional antidepressant treatments. 30cm.

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Evaluating the Synergistic Role of Insulin and Photobiomodulation in alleviating Diabetic Neuropathy and Cognitive Impairment /

By Kayani, Hooreen . . 88p. , Diabetic neuropathy and cognitive impairment are debilitating complications of diabetes, yet effective multi-targeted therapies remain limited. This study investigated the synergistic effects of Insulin and Photobiomodulation (PBM) in a streptozotocin (STZ) induced diabetic mouse model. Mice were divided into five groups: healthy control, diseased, PBM-treated, Insulintreated, and PBM + Insulin-treated, and received treatments for seven days. Functional outcomes were assessed through behavioural and biochemical analyses, while histopathological and molecular evaluations examined tissue integrity and the expression of neuroprotective markers, including Brain-derived Neurotrophic Factor (BDNF) and Myelin Protein Zero (MPZ), with β-actin as a reference. The combination of PBM and Insulin produced the most pronounced improvements, demonstrating enhanced cognitive performance, reduced neuropathic pain, and preservation of neuronal structure, peripheral nerve integrity, and multi-organ morphology, including the brain, sciatic nerve, heart, liver, kidney, and lungs. PBM or Insulin alone provided partial protection, with moderate amelioration of functional deficits and tissue pathology. Mechanistically, combination therapy upregulated BDNF and MPZ expression, suggesting a molecular basis for enhanced neuroprotection and remyelination. These findings highlight the potential of PBM combined with Insulin as a synergistic intervention to mitigate diabetes-induced neuropathy and cognitive decline. Incorporating such multi-modal strategies may offer a promising avenue for managing diabetes-related multi-organ complications and improving overall outcomes in diabetic patients. 30cm.

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CDCA-Bound Carbon-Based Nanoparticles for the Treatment of Cognitive Impairment and Neuropathy Associated with Diabetes Mellitus /

By Noreen, Samra . . 99p. , Diabetes Mellitus (DM) is a severe metabolic disorder defined by hyperglycemia, which leads to cognitive impairment and neuropathy. It is characterized by chronic pain, sensory loss, impaired motor coordination, and cognitive decline. According to the WHO (2024) and International Diabetes Federation (IDF) statistics, neuropathy affects over 50% of people with type 1 and type 2 diabetes. Current treatments for diabetic neuropathy provide only partial relief and fail to stop neurodegeneration, highlighting the need for novel strategies that both restore metabolic balance and protect neural function. Chenodeoxycholic acid (CDCA), a primary bile acid with antiinflammatory and neuroprotective effects, is limited by toxicity at high doses. CDs, owing to their ultra-small size, biocompatibility, and blood-brain barrier (BBB) permeability, are ideal for treating diabetic neuropathy and cognitive impairment. N-doped CDs were synthesized hydrothermally and conjugated with CDCA via carbodimide coupling. FTIR confirmed preserved functional groups, while UV-Vis showed π–π stacking and hydrogen bonding. Hemocompatibility testing revealed <5% hemolysis, confirming blood safety. Drug loading efficiency was ~ 99.6% (2489.82 bound from 2500 µg). Sustained release analysis showed ~ 17% release at 24 h and ~ 29% over 7 days without a burst effect. In-vivo, diabetic mice were grouped into control, free CDCA, CDCA-NCDs, and insulin glargine. The nanoconjugate was administered at a dose of 10 mg/kg on day 1 st, 7th and 14th compared to daily free CDCA. Behavioral tests (nociception, anxiety, and cognition) showed significant improvements (p < 0.05-0.0001) with CDCA-NCDs. Glycemic control, weight, and histopathology also favored CDCA-NCDs over free CDCA. Overall, CDCA-NCDs demonstrated excellent safety, efficient drug loading, controlled release, and superior therapeutic outcomes, supporting them as a promising low-frequency dosing strategy for neuroprotection and metabolic regulation in diabetic neuropathy. 30cm.

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Cinnamon-derived Carbon Dots as Therapeutic Intervention for Cognitive Impairment and Neuropathy Associated With Diabetes /

By Hadiqa Shahid. . 151p. , Diabetes mellitus, a chronic metabolic disorder affecting over 589 million adults globally, induces diabetes-associated cognitive impairment and peripheral neuropathy through sustained hyperglycemia, oxidative stress, neuroinflammation, and blood-brain barrier dysfunction. Existing therapies inadequately target both central and peripheral neural damage due to poor blood-brain barrier penetration. This study developed cinnamon barkderived carbon nanodots (CIN-CNDs) conjugated with chenodeoxycholic acid (CINCDCA) via green hydrothermal synthesis as a novel nanotherapeutic for diabetesassociated complications. Characterization using UV-Visible spectroscopy, Fourier Transform Infrared spectroscopy (FTIR), Atomic Force Microscopy (AFM), and Scanning Electron Microscopy (SEM) confirmed nanoscale particle formation (average 4.4 nm), successful functionalization, and surface morphology suitable for biomedical applications. Physicochemical testing demonstrated excellent hemocompatibility (<5% hemolysis), high drug loading efficiency (85 ± 3%), pH-stable hydrolytic stability across physiological ranges, and controlled sustained release profile over 72 hours. In streptozotocin-induced diabetic mice, CIN-CDCA nanoconjugates (10 mg/kg, i.p., 1, 4, 14 days) showed significant improvements across comprehensive neuropathic pain assessments (cold allodynia, hot plate, paw pressure, tail immersion; all p<0.01) and cognitive function tests (Morris water maze, Y-maze, novel object recognition, open field).CIN-CDCA nanoconjugates demonstrate biocompatibility, targeted delivery, and disease-modifying efficacy for diabetes-associated neural complications, warranting clinical translation. 30cm.

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