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Article ; Online: Common Sleep Disorders in Children.

Deshpande, Prajakta / Salcedo, Betzy / Haq, Cynthia

2022 Volume 105, Issue 2, Page(s) 168–176

Abstract: Childhood sleep disorders can disrupt family dynamics and cause cognitive and behavior problems. Early recognition and management can prevent these complications. Behavior subtypes of childhood insomnias affect 10% to 30% of children and result from ... ...

Abstract	Childhood sleep disorders can disrupt family dynamics and cause cognitive and behavior problems. Early recognition and management can prevent these complications. Behavior subtypes of childhood insomnias affect 10% to 30% of children and result from inconsistent parental limit-setting and improper sleep-onset association. Behavior insomnias are treated using extinction techniques and parent education. Hypnotic medications are not recommended. Obstructive sleep apnea affects 1% to 5% of children. Polysomnography is required to diagnose obstructive sleep apnea; history and physical examination alone are not adequate. Adenotonsillectomy is the first-line treatment for obstructive sleep apnea. Nasal continuous positive airway pressure is the second-line treatment for children who do not respond to surgery or if adenotonsillectomy is contraindicated. Restless legs syndrome can be difficult to recognize and has an association with attention-deficit/hyperactivity disorder. Management of restless legs syndrome includes treatment of iron deficiency, if identified, and removal of triggering factors. Parasomnias affect up to 50% of children and usually resolve spontaneously by adolescence. Management of parasomnias involves parental education, reassurance, safety precautions, and treating comorbid conditions. Delayed sleep phase syndrome is found during adolescence, manifesting as a night owl preference. Treatment of delayed sleep phase syndrome includes sleep hygiene, nighttime melatonin, and morning bright light exposure. Sleep deprivation is of increasing concern, affecting 68% of people in high school.
MeSH term(s)	Continuous Positive Airway Pressure ; Humans ; Parasomnias/diagnosis ; Polysomnography/methods ; Sleep Apnea, Obstructive/therapy ; Sleep Wake Disorders
Language	English
Publishing date	2022-02-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	412694-4
ISSN	1532-0650 ; 0002-838X ; 0572-3612
ISSN (online)	1532-0650
ISSN	0002-838X ; 0572-3612
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Article: Signaling interactions among neurons impact cell fitness and death in Alzheimer's disease.

Yeates, Catherine / Deshpande, Prajakta / Kango-Singh, Madhuri / Singh, Amit

Neural regeneration research

2022 Volume 18, Issue 4, Page(s) 784–789

Abstract: The pathology of Alzheimer's disease involves a long preclinical period, where the characteristic clinical symptoms of the changes in the brain are undetectable. During the preclinical period, homeostatic mechanisms may help prevent widespread cell death. ...

Abstract	The pathology of Alzheimer's disease involves a long preclinical period, where the characteristic clinical symptoms of the changes in the brain are undetectable. During the preclinical period, homeostatic mechanisms may help prevent widespread cell death. Evidence has pointed towards selective cell death of diseased neurons playing a potentially protective role. As the disease progresses, dysregulation of signaling pathways that govern cell death contributes to neurodegeneration. Aberrant activation of the c-Jun N-terminal kinase pathway has been established in human and animal models of Alzheimer's disease caused by amyloid-beta 42- or tau-mediated neurodegeneration. Clonal mosaic studies in Drosophila that examine amyloid-beta 42 in a subset of neurons suggest complex interplay between amyloid-beta 42-expressing and wild-type cells. This review examines the role of c-Jun N-terminal kinase signaling in the context of cell competition and short-range signaling interactions between amyloid-beta 42-expressing and wild-type neurons. Cell competition is a conserved phenomenon regulating tissue integrity by assessing the fitness of cells relative to their neighbors and eliminating suboptimal cells. Somatic clones of amyloid-beta 42 that juxtapose genetically distinct neuronal cell populations show promise for studying neurodegeneration. Generating genetic mosaics with labeled clones of amyloid-beta 42- or tau-expressing and wild-type neurons will allow us to understand how short-range signaling alterations trigger cell death in neurons and thereby contribute to the progression of Alzheimer's disease. These approaches have the potential to uncover biomarkers for early Alzheimer's disease detection and new therapeutic targets for intervention.
Language	English
Publishing date	2022-10-17
Publishing country	India
Document type	Journal Article
ZDB-ID	2388460-5
ISSN	1876-7958 ; 1673-5374
ISSN (online)	1876-7958
ISSN	1673-5374
DOI	10.4103/1673-5374.354516
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Article ; Online: Protocol to study cell death using TUNEL assay in

Chimata, Anuradha Venkatakrishnan / Deshpande, Prajakta / Mehta, Abijeet Singh / Singh, Amit

STAR protocols

2022 Volume 3, Issue 1, Page(s) 101140

Abstract: Cell death maintains tissue homeostasis by eliminating dispensable cells. Misregulation of cell death is seen in diseases like cancer, neurodegeneration, etc. Therefore, cell death assays like TUNEL have become reliable tools, where fragmented DNA of ... ...

Abstract	Cell death maintains tissue homeostasis by eliminating dispensable cells. Misregulation of cell death is seen in diseases like cancer, neurodegeneration, etc. Therefore, cell death assays like TUNEL have become reliable tools, where fragmented DNA of dying cells gets fluorescently labeled and can be detected under microscope. We used TUNEL assay in
MeSH term(s)	Animals ; Apoptosis ; Drosophila/genetics ; Drosophila melanogaster ; Imaginal Discs ; In Situ Nick-End Labeling
Language	English
Publishing date	2022-01-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2666-1667
ISSN (online)	2666-1667
DOI	10.1016/j.xpro.2022.101140
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Article ; Online: N-Acetyltransferase 9 ameliorates Aβ42-mediated neurodegeneration in the Drosophila eye.

Deshpande, Prajakta / Chimata, Anuradha Venkatakrishnan / Snider, Emily / Singh, Aditi / Kango-Singh, Madhuri / Singh, Amit

Cell death & disease

2023 Volume 14, Issue 7, Page(s) 478

Abstract: Alzheimer's disease (AD), a progressive neurodegenerative disorder, manifests as accumulation of amyloid-beta-42 (Aβ42) plaques and intracellular accumulation of neurofibrillary tangles (NFTs) that results in microtubule destabilization. Targeted ... ...

Abstract	Alzheimer's disease (AD), a progressive neurodegenerative disorder, manifests as accumulation of amyloid-beta-42 (Aβ42) plaques and intracellular accumulation of neurofibrillary tangles (NFTs) that results in microtubule destabilization. Targeted expression of human Aβ42 (GMR > Aβ42) in developing Drosophila eye retinal neurons results in Aβ42 plaque(s) and mimics AD-like extensive neurodegeneration. However, there remains a gap in our understanding of the underlying mechanism(s) for Aβ42-mediated neurodegeneration. To address this gap in information, we conducted a forward genetic screen, and identified N-acetyltransferase 9 (Mnat9) as a genetic modifier of GMR > Aβ42 neurodegenerative phenotype. Mnat9 is known to stabilize microtubules by inhibiting c-Jun-N- terminal kinase (JNK) signaling. We found that gain-of-function of Mnat9 rescues GMR > Aβ42 mediated neurodegenerative phenotype whereas loss-of-function of Mnat9 exhibits the converse phenotype of enhanced neurodegeneration. Here, we propose a new neuroprotective function of Mnat9 in downregulating the JNK signaling pathway to ameliorate Aβ42-mediated neurodegeneration, which is independent of its acetylation activity. Transgenic flies expressing human NAT9 (hNAT9), also suppresses Aβ42-mediated neurodegeneration thereby suggesting functional conservation in the interaction of fly Mnat9 or hNAT9 with JNK-mediated neurodegeneration. These studies add to the repertoire of molecular mechanisms that mediate cell death response following accumulation of Aβ42 and may provide new avenues for targeting neurodegeneration.
MeSH term(s)	Animals ; Humans ; Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Amyloid beta-Peptides/genetics ; Amyloid beta-Peptides/metabolism ; Disease Models, Animal ; Drosophila/genetics ; Drosophila/metabolism ; Drosophila melanogaster/genetics ; Drosophila melanogaster/metabolism ; Peptide Fragments/metabolism ; JNK Mitogen-Activated Protein Kinases ; Acetyltransferases
Chemical Substances	Amyloid beta-Peptides ; amyloid beta-protein (1-42) ; Peptide Fragments ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Acetyltransferases (EC 2.3.1.-)
Language	English
Publishing date	2023-07-28
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-023-05973-z
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Article ; Online: Impact of RASSF1A gene methylation on clinico-pathological features of tumor and non-tumor tissue of breast cancer.

Gupta, Vivek / Agarwal, Prerna / Deshpande, Prajakta

Annals of diagnostic pathology

2021 Volume 52, Page(s) 151722

Abstract: Background: Breast cancer is the most common malignancy in women caused by genetic and epigenetic changes. Promoter DNA methylation in tumor suppressor gene plays a major role in breast cancer. The study determined the association of promoter DNA ... ...

Abstract	Background: Breast cancer is the most common malignancy in women caused by genetic and epigenetic changes. Promoter DNA methylation in tumor suppressor gene plays a major role in breast cancer. The study determined the association of promoter DNA methylation of RASSF1A gene with clinicopathological features in tumor and non-tumor tissue. Materials and methods: A cross sectional study was conducted in the Department of Pathology, Government Institute of Medical Sciences, Greater Noida and Molecular Pathology Laboratory, Department of Pathology, Jawaharlal Nehru Medical College, Datta Meghe Institute of Medical Sciences. Two sections, one from tumor and the other from non-tumor tissue, were obtained and processed for DNA extraction and bisulphite conversion. Methylation specific PCR was done and results of RASSF1A promoter methylation were statistically correlated with clinicopathological features. Results: Of the 27 breast cancer tissue, 22 showed invasive ductal carcinoma, one showed invasive lobular carcinoma, another showed ductal carcinoma in situ and three cases showed malignant phyllodes tumor of breast. DNA promoter methylation was found in all the cases. 93% of tumor tissue samples and 67% of the non-tumor tissue samples were found to be aberrantly methylated. Tumor size and histological grade were found to be significantly (p-val <0.05) associated with the RASSF1A gene promoter methylation. Conclusion: A significant association of higher tumor size and tumor histological grade with promoter methylation of RASSF1A gene exists suggestive of its being an important determinant of prognostic staging. This critical event in tumorigenesis may be of clinical utility in assessing breast cancer progression. Micro abstract: The study focuses on the RASSF1A gene promoter methylation and its impact on the clinicopathological features in Indian breast cancer patients highlighting the differences from other genetically different population. We found that RASFF1A gene methylation has significant impact on tumor size and tumor grade. The work carries high significance because it addresses the DNA methylation of tumor suppressor gene in relevance of breast cancer. It may also be the first such report on Indian patients with breast cancer.
MeSH term(s)	Adult ; Aged ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Carcinogenesis/genetics ; Carcinogenesis/pathology ; Carcinoma, Ductal, Breast/diagnosis ; Carcinoma, Ductal, Breast/epidemiology ; Carcinoma, Ductal, Breast/pathology ; Carcinoma, Intraductal, Noninfiltrating/diagnosis ; Carcinoma, Intraductal, Noninfiltrating/epidemiology ; Carcinoma, Intraductal, Noninfiltrating/pathology ; Carcinoma, Lobular/diagnosis ; Carcinoma, Lobular/epidemiology ; Carcinoma, Lobular/pathology ; Cross-Sectional Studies ; DNA Methylation ; Disease Progression ; Epigenesis, Genetic/genetics ; Female ; Humans ; India/epidemiology ; Middle Aged ; Neoplasm Invasiveness/pathology ; Neoplasm Staging/methods ; Phyllodes Tumor/diagnosis ; Phyllodes Tumor/epidemiology ; Phyllodes Tumor/pathology ; Prognosis ; Promoter Regions, Genetic/genetics ; Tumor Suppressor Proteins/genetics
Chemical Substances	RASSF1 protein, human ; Tumor Suppressor Proteins
Language	English
Publishing date	2021-02-11
Publishing country	United States
Document type	Comparative Study ; Journal Article
ZDB-ID	1440011-x
ISSN	1532-8198 ; 1092-9134
ISSN (online)	1532-8198
ISSN	1092-9134
DOI	10.1016/j.anndiagpath.2021.151722
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Article ; Online: Unbiased automated quantitation of ROS signals in live retinal neurons of

Deshpande, Prajakta / Gogia, Neha / Chimata, Anuradha Venkatakrishnan / Singh, Amit

BioTechniques

2021 Volume 71, Issue 2, Page(s) 416–424

Abstract: Numerous imaging modules are utilized to study changes that occur during cellular processes. Besides qualitative (immunohistochemical) or semiquantitative (Western blot) approaches, direct quantitation method(s) for detecting and analyzing signal ... ...

Abstract	Numerous imaging modules are utilized to study changes that occur during cellular processes. Besides qualitative (immunohistochemical) or semiquantitative (Western blot) approaches, direct quantitation method(s) for detecting and analyzing signal intensities for disease(s) biomarkers are lacking. Thus, there is a need to develop method(s) to quantitate specific signals and eliminate noise during live tissue imaging. An increase in reactive oxygen species (ROS) such as superoxide (O
MeSH term(s)	Animals ; Automation ; Drosophila ; Fluorescence ; Reactive Oxygen Species ; Retinal Neurons
Chemical Substances	Reactive Oxygen Species
Language	English
Publishing date	2021-08-05
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	48453-2
ISSN	1940-9818 ; 0736-6205
ISSN (online)	1940-9818
ISSN	0736-6205
DOI	10.2144/btn-2021-0006
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Article: SARS-CoV2 Nsp3 protein triggers cell death and exacerbates amyloid β42-mediated neurodegeneration.

Singh, Aditi / Chimata, Anuradha Venkatakrishnan / Deshpande, Prajakta / Bajpai, Soumya / Sangeeth, Anjali / Rajput, Mrigendra / Singh, Amit

Neural regeneration research

2023 Volume 19, Issue 6, Page(s) 1385–1392

Language	English
Publishing date	2023-08-14
Publishing country	India
Document type	Journal Article
ZDB-ID	2388460-5
ISSN	1876-7958 ; 1673-5374
ISSN (online)	1876-7958
ISSN	1673-5374
DOI	10.4103/1673-5374.382989
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Article ; Online: miR-277 targets the proapoptotic gene-hid to ameliorate Aβ42-mediated neurodegeneration in Alzheimer's model.

Deshpande, Prajakta / Chen, Chao-Yi / Chimata, Anuradha Venkatakrishnan / Li, Jian-Chiuan / Sarkar, Ankita / Yeates, Catherine / Chen, Chun-Hong / Kango-Singh, Madhuri / Singh, Amit

Cell death & disease

2024 Volume 15, Issue 1, Page(s) 71

Abstract: Alzheimer's disease (AD), an age-related progressive neurodegenerative disorder, exhibits reduced cognitive function with no cure to date. One of the reasons for AD is the accumulation of Amyloid-beta 42 (Aβ42) plaque(s) that trigger aberrant gene ... ...

Abstract	Alzheimer's disease (AD), an age-related progressive neurodegenerative disorder, exhibits reduced cognitive function with no cure to date. One of the reasons for AD is the accumulation of Amyloid-beta 42 (Aβ42) plaque(s) that trigger aberrant gene expression and signaling, which results in neuronal cell death by an unknown mechanism(s). Misexpression of human Aβ42 in the developing retina of Drosophila exhibits AD-like neuropathology. Small non-coding RNAs, microRNAs (miRNAs), post-transcriptionally regulate the expression of their target genes and thereby regulate different signaling pathways. In a forward genetic screen, we identified miR-277 (human ortholog is hsa-miR-3660) as a genetic modifier of Aβ42-mediated neurodegeneration. Loss-of-function of miR-277 enhances the Aβ42-mediated neurodegeneration. Whereas gain-of-function of miR-277 in the GMR > Aβ42 background downregulates cell death to maintain the number of neurons and thereby restores the retinal axonal targeting defects indicating the functional rescue. In addition, gain-of-function of miR-277 rescues the eclosion- and climbing assays defects observed in GMR > Aβ42 background. Thus, gain-of-function of miR-277 rescues both structurally as well as functionally the Aβ42-mediated neurodegeneration. Furthermore, we identified head involution defective (hid), an evolutionarily conserved proapoptotic gene, as one of the targets of miR-277 and validated these results using luciferase- and qPCR -assays. In the GMR > Aβ42 background, the gain-of-function of miR-277 results in the reduction of hid transcript levels to one-third of its levels as compared to GMR > Aβ42 background alone. Here, we provide a novel molecular mechanism where miR-277 targets and downregulates proapoptotic gene, hid, transcript levels to rescue Aβ42-mediated neurodegeneration by blocking cell death. These studies shed light on molecular mechanism(s) that mediate cell death response following Aβ42 accumulation seen in neurodegenerative disorders in humans and provide new therapeutic targets for neurodegeneration.
MeSH term(s)	Animals ; Humans ; Alzheimer Disease/metabolism ; Amyloid beta-Peptides/genetics ; Amyloid beta-Peptides/metabolism ; Neurons/metabolism ; Axons/metabolism ; Drosophila/metabolism ; MicroRNAs/metabolism ; Peptide Fragments/metabolism
Chemical Substances	Amyloid beta-Peptides ; MicroRNAs ; Peptide Fragments ; MIRN277 microRNA, Drosophila
Language	English
Publishing date	2024-01-18
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-023-06361-3
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Article: Exploring the efficacy of natural products in alleviating Alzheimer's disease.

Deshpande, Prajakta / Gogia, Neha / Singh, Amit

Neural regeneration research

2019 Volume 14, Issue 8, Page(s) 1321–1329

Abstract: Alzheimer's disease (hereafter AD) is a progressive neurodegenerative disorder that affects the central nervous system. There are multiple factors that cause AD, viz., accumulation of extracellular Amyloid-beta 42 plaques, intracellular hyper- ... ...

Abstract	Alzheimer's disease (hereafter AD) is a progressive neurodegenerative disorder that affects the central nervous system. There are multiple factors that cause AD, viz., accumulation of extracellular Amyloid-beta 42 plaques, intracellular hyper-phosphorylated Tau tangles, generation of reactive oxygen species due to mitochondrial dysfunction and genetic mutations. The plaques and tau tangles trigger aberrant signaling, which eventually cause cell death of the neurons. As a result, there is shrinkage of brain, cognitive defects, behavioral and psychological problems. To date, there is no direct cure for AD. Thus, scientists have been testing various strategies like screening for the small inhibitor molecule library or natural products that may block or prevent onset of AD. Historically, natural products have been used in many cultures for the treatment of various diseases. The research on natural products have gained importance as the active compounds extracted from them have medicinal values with reduced side effects, and they are bioavailable. The natural products may target the proteins or members of signaling pathways that get altered in specific diseases. Many natural products are being tested in various animal model systems for their role as a potential therapeutic target for AD, and to address questions about how these natural products can rescue AD or other neurodegenerative disorders. Some of these products are in clinical trials and results are promising because of their neuroprotective, anti-inflammatory, antioxidant, anti-amyloidogenic, anticholinesterase activities and easy availability. This review summarizes the use of animal model systems to identify natural products, which may serve as potential therapeutic targets for AD.
Language	English
Publishing date	2019-04-09
Publishing country	India
Document type	Journal Article ; Review
ZDB-ID	2388460-5
ISSN	1876-7958 ; 1673-5374
ISSN (online)	1876-7958
ISSN	1673-5374
DOI	10.4103/1673-5374.253509
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Article ; Online: Newt regeneration genes regulate Wingless signaling to restore patterning in

Mehta, Abijeet Singh / Deshpande, Prajakta / Chimata, Anuradha Venkatakrishnan / Tsonis, Panagiotis A / Singh, Amit

iScience

2021 Volume 24, Issue 10, Page(s) 103166

Abstract: Newts utilize their unique genes to restore missing parts by strategic regulation of conserved signaling pathways. Lack of genetic tools poses challenges to determine the function of such genes. Therefore, we used ... ...

Abstract	Newts utilize their unique genes to restore missing parts by strategic regulation of conserved signaling pathways. Lack of genetic tools poses challenges to determine the function of such genes. Therefore, we used the
Language	English
Publishing date	2021-09-24
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2021.103166
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