Browsing by Author "Perveen, Asma"

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Editorial: The Alzheimer’s Disease Challenge, Volume II
(Frontier Scientific Publishing, 2023-01-10) Kamal, Mohammad Amjad; Alexiou, Athanasios; Perveen, Asma
Data analysis obtained from the 2019 Global Burden of Disease (GBD) database, the numbers and age-standardized rates (ASRs) of incidence, prevalence, death, and disability-adjusted life-years (DALYs) of AD and other dementias from 1990 to 2019 by Li X. et al. support the emerging necessity of supporting health strategies for more effective prevention and treatment measures in a rapidly increasing aging population. Li X. et al. identified a constantly increasing incidence and prevalence of AD and other dementias over these 30 years. Furthermore, the risk of developing dementia is proportional to age, with females and the elderly having a higher risk. Additionally, the researchers identified smoking as a significant risk factor for the disease burden, and the age-standardized rates (ASRs) of incidence, prevalence, and disability-adjusted life-years (DALYs) were positively correlated with the sociodemographic index (SDI) (Li X. et al.).
Emerging Promise of Therapeutic Approaches Targeting Mitochondria in Neurodegenerative Disorders
(Emerald Publishing Limited, 2023-04-12) Rahman, Md Mominur; Tumpa, Mst Afroza Alam; Rahaman, Md Saidur; Islam, Fahadul; Islam, Fahadul; Sutradhar, Popy Rani; Ahmed, Muniruddin; Alghamdi, Badrah S.; Hafeez, Abdul; Alexiou, Athanasios; Perveen, Asma; Ashraf, Ghulam Md
Mitochondria are critical for homeostasis and metabolism in all cellular eukaryotes. Brain mitochondria are the primary source of fuel that supports many brain functions, including intracellular energy supply, cellular calcium regulation, regulation of limited cellular oxidative capacity, and control of cell death. Much evidence suggests that mitochondria play a central role in neurodegenerative disorders (NDDs) such as Parkinson's disease, Alzheimer's disease, Huntington's disease, and amyotrophic lateral sclerosis. Ongoing studies of NDDs have revealed that mitochondrial pathology is mainly found in inherited or irregular NDDs and is thought to be associated with the pathophysiological cycle of these disorders. Typical mitochondrial disturbances in NDDs include increased free radical production, decreased ATP synthesis, alterations in mitochondrial permeability, and mitochondrial DNA damage. The main objective of this review is to highlight the basic mitochondrial problems that occur in NDDs and discuss the use mitochondrial drugs, especially mitochondrial antioxidants, mitochondrial permeability transition blockade, and mitochondrial gene therapy, for the treatment and control of NDDs.
Hutchinson-Gilford Progeria Syndrome
(Scopus, 2021) Rahman, Md Mominur; Ferdous, Kazi Sayma; Ahmed, Muniruddin; Islam, Mohammad Touhidul; Khan, Md Robin; Perveen, Asma; Ashraf, Ghulam Md; Uddin, Md Sahab
Lamin A/C encoded by the LMNA gene is an essential component for maintaining the nuclear structure. Mutation in the lamin A/C leads to a group of inherited disorders is known as laminopathies. In the human body, there are several mutations in the LMNA gene that have been identified. It can affect diverse organs or tissues or can be systemic, causing different diseases. In this review, we mainly focused on one of the most severe laminopathies, Hutchinson-Gilford progeria syndrome (HGPS). HGPS is an immensely uncommon, deadly, metameric ill-timed laminopathies caused by the abnormal splicing of the LMNA gene and production of an aberrant protein known as progerin. Here, we also presented the currently available data on the molecular mechanism, pathophysiology, available treatment, and future approaches to this deadly disease. Due to the production of progerin, an abnormal protein leads to an abnormality in nuclear structure, defects in DNA repair, shortening of telomere, and impairment in gene regulation which ultimately results in aging in the early stage of life. Now some treatment options are available for this disease, but a proper understanding of the molecular mechanism of this disease will help to develop a more appropriate treatment which makes it an emerging area of research.
Natural products in the management of neurodegenerative diseases
(2024-05-16) Rajat, Goyal; Mittal, Pooja; Gautam, Rupesh K.; Kamal, Mohammad Amjad; Perveen, Asma; Garg, Vandana; Alexiou, Athanasios; Saboor, Muhammad; Haque, Shafiul; Farhana, Aisha; Papadakis, Marios; Ashraf, Ghulam Md
Neurodegenerative diseases represent one of the utmost imperative well-being health issues and apprehensions due to their escalating incidence of mortality. Natural derivatives are more efficacious in various preclinical models of neurodegenerative illnesses. These natural compounds include phytoconstituents in herbs, vegetables, fruits, nuts, and marine and freshwater flora, with remarkable efficacy in mitigating neurodegeneration and enhancing cognitive abilities in preclinical models. According to the latest research, the therapeutic activity of natural substances can be increased by adding phytoconstituents in nanocarriers such as nanoparticles, nanogels, and nanostructured lipid carriers. They can enhance the stability and specificity of the bioactive compounds to a more considerable extent. Nanotechnology can also provide targeting, enhancing their specificity to the respective site of action. In light of these findings, this article discusses the biological and therapeutic potential of natural products and their bioactive derivatives to exert neuroprotective effects and some clinical studies assessing their translational potential to treat neurodegenerative disorders.
Natural Products in the Management of Neurodegenerative Diseases
(Springer Nature, 2024-05-16) Goyal, Rajat; Mittal, Pooja; Gautam, Rupesh K.; Kamal, Mohammad Amjad; Perveen, Asma; Garg, Vandana; Alexiou, Athanasios; Saboor, Muhammad; Haque, Shafiul; Farhana, Aisha; Papadakis, Marios; Ashraf, Ghulam Md
"Neurodegenerative diseases represent one of the utmost imperative well-being health issues and apprehensions due to their escalating incidence of mortality. Natural derivatives are more efficacious in various preclinical models of neurodegenerative illnesses. These natural compounds include phytoconstituents in herbs, vegetables, fruits, nuts, and marine and freshwater flora, with remarkable efficacy in mitigating neurodegeneration and enhancing cognitive abilities in preclinical models. According to the latest research, the therapeutic activity of natural substances can be increased by adding phytoconstituents in nanocarriers such as nanoparticles, nanogels, and nanostructured lipid carriers. They can enhance the stability and specificity of the bioactive compounds to a more considerable extent. Nanotechnology can also provide targeting, enhancing their specificity to the respective site of action. In light of these findings, this article discusses the biological and therapeutic potential of natural products and their bioactive derivatives to exert neuroprotective effects and some clinical studies assessing their translational potential to treat neurodegenerative disorders. Graphical Abstract Common mechanisms, therapeutic targets, and molecular pathogenesis of neurodegeneration. It is focused on the biological and therapeutic potential of natural products and their bioactive derivatives to exert a neuroprotective effect on the pathologies of neurodegenerative diseases."
Repurposing Food Molecules as a Potential BACE1 Inhibitor for Alzheimer's Disease
(Daffodil International University, 2022-08-22) Mukerjee, Nobendu; Das, Anubhab; Jawarkar, Rahul D.; Maitra, Swastika; Das, Padmashree; Castrosanto, Melvin A.; Paul, Soumyadip; Samad, Abdul; Zaki, Magdi E. A.; Al-Hussain, Sami A.; Masand, Vijay H.; Hasan, Mohammad Mehedi; Bukhari, Syed Nasir Abbas; Perveen, Asma; Alghamdi, Badrah S.; Alexiou, Athanasios; Kamal, Mohammad Amjad; Dey, Abhijit; Malik, Sumira; Bakal, Ravindra L.; Abuzenadah, Adel Mohammad; Ghosh, Arabinda; Ashraf, Ghulam Md
Alzheimer’s disease (AD) is a severe neurodegenerative disorder of the brain that manifests as dementia, disorientation, difficulty in speech, and progressive cognitive and behavioral impairment. The emerging therapeutic approach to AD management is the inhibition of β-site APP cleaving enzyme-1 (BACE1), known to be one of the two aspartyl proteases that cleave β-amyloid precursor protein (APP). Studies confirmed the association of high BACE1 activity with the proficiency in the formation of β-amyloid-containing neurotic plaques, the characteristics of AD. Only a few FDA-approved BACE1 inhibitors are available in the market, but their adverse off-target effects limit their usage. In this paper, we have used both ligand-based and target-based approaches for drug design. The QSAR study entails creating a multivariate GA-MLR (Genetic Algorithm-Multilinear Regression) model using 552 molecules with acceptable statistical performance (R2 = 0.82, Q2loo = 0.81). According to the QSAR study, the activity has a strong link with various atoms such as aromatic carbons and ring Sulfur, acceptor atoms, sp2-hybridized oxygen, etc. Following that, a database of 26,467 food compounds was primarily used for QSAR-based virtual screening accompanied by the application of the Lipinski rule of five; the elimination of duplicates, salts, and metal derivatives resulted in a truncated dataset of 8,453 molecules. The molecular descriptor was calculated and a well-validated 6-parametric version of the QSAR model was used to predict the bioactivity of the 8,453 food compounds. Following this, the food compounds whose predicted activity (pKi) was observed above 7.0 M were further docked into the BACE1 receptor which gave rise to the Identification of 4-(3,4-Dihydroxyphenyl)-2-hydroxy-1H-phenalen-1-one (PubChem I.D: 4468; Food I.D: FDB017657) as a hit molecule (Binding Affinity = −8.9 kcal/mol, pKi = 7.97 nM, Ki = 10.715 M). Furthermore, molecular dynamics simulation for 150 ns and molecular mechanics generalized born and surface area (MMGBSA) study aided in identifying structural motifs involved in interactions with the BACE1 enzyme. Molecular docking and QSAR yielded complementary and congruent results. The validated analyses can be used to improve a drug/lead candidate’s inhibitory efficacy against the BACE1. Thus, our approach is expected to widen the field of study of repurposing nutraceuticals into neuroprotective as well as anti-cancer and anti-viral therapeutic interventions.
Resveratrol and Neuroprotection
(Daffodil International University, 2022-05-12) Islam, Fahadul; Nafady, Mohamed H.; Islam, Md. Rezaul; Saha, Susmita; Rashid, Salma; Akter, Aklima; Rashid, Md. Harun‑ Or‑; Akhtar, Muhammad Furqan; Perveen, Asma; Ashraf, Ghulam Md.; Rahman, Md. Habibur; Sweilam, Sherouk Hussein
Alzheimer’s disease (AD) is the most common cause of dementia and cognitive impairment; yet, there is currently no treatment. A buildup of Aβ, tau protein phosphorylation, oxidative stress, and inflammation in AD is pathogenic. The accumulation of amyloid-beta (Aβ) peptides in these neurocognitive areas is a significant characteristic of the disease. Therefore, inhibiting Aβ peptide aggregation has been proposed as the critical therapeutic approach for AD treatment. Resveratrol has been demonstrated in multiple studies to have a neuroprotective, anti-inflammatory, and antioxidant characteristic and the ability to minimize Aβ peptides aggregation and toxicity in the hippocampus of Alzheimer’s patients, stimulating neurogenesis and inhibiting hippocampal degeneration. Furthermore, resveratrol’s antioxidant effect promotes neuronal development by activating the silent information regulator-1 (SIRT1), which can protect against the detrimental effects of oxidative stress. Resveratrol-induced SIRT1 activation is becoming more crucial in developing novel therapeutic options for AD and other diseases that have neurodegenerative characteristics. This review highlighted a better knowledge of resveratrol’s mechanism of action and its promising therapeutic efficacy in treating AD. We also highlighted