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1. Solubilisation & purification of membrane proteins using benzylamine-modified SMA polymers

Author

Akram, Aneel, Hadasha, Waled, Kuyler, Gestél C., Smith, Michael-Phillip, Bailey-Dallaway, Shauna, Preedy, Aiden, Browne, Caolan, Broadbent, Luke, Hill, Adam, Javaid, Tahreem, Nazar, Haroon, Samra, Nikita, Naveed, Anadil, Tregunna, Holly, Joshi, Hetal, Akhtar, Nusheen, Javed, Aneesa, Bowater, Jessica, Ravenhill, Joel, Hajdu, Patrik, Ali, Yazdan, Tailor, Yanik, Mumtaz, Sabreen, Hamza, Mohammed, Gill, Kiran, Gillett, Jemma, Patton, Faye, Arshid, Huma, Zaheer, Maria, Qureshi, Hannah, Edwards, Isabel, Patel, Shreya, Azadi, Aaminah, Pollock, Naomi, Kitchen, Philip, Klumperman, Bert, and Rothnie, Alice J.

Published
2025
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2. Frequency-potency analysis of IgG+ memory B cells delineates neutralizing antibody responses at single-cell resolution

Author

Tenggara, Michelle K., Oh, Seo-Ho, Yang, Catherine, Nariya, Hardik K., Metz, Amanda M., Upadhyay, Amit A., Gudipati, Dedeepya R., Guo, Lizheng, McGhee, Emily G., Gill, Kiran, Viox, Elise G., Mason, Rosemarie D., Doria-Rose, Nicole A., Foulds, Kathryn E., Mascola, John R., Du, Yuhong, Fu, Haian, Altman, John D., Yan, Qi, Sheng, Zizhang, Bosinger, Steven E., and Kong, Rui

Published
2024
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3. Limited impact of fingolimod treatment during the initial weeks of ART in SIV-infected rhesus macaques

Author

Pino, Maria, Pagliuzza, Amélie, Pampena, M. Betina, Deleage, Claire, Viox, Elise G., Nguyen, Kevin, Shim, Inbo, Zhang, Adam, Harper, Justin L., Samer, Sadia, King, Colin T., Cervasi, Barbara, Gill, Kiran P., Ehnert, Stephanie, Jean, Sherrie M., Freeman, Michael L., Lifson, Jeffrey D., Kulpa, Deanna, Betts, Michael R., Chomont, Nicolas, Lederman, Michael M., and Paiardini, Mirko

Published
2022
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4. Antibiotics-Driven Gut Microbiome Perturbation Alters Immunity to Vaccines in Humans

Author

Hagan, Thomas, Cortese, Mario, Rouphael, Nadine, Boudreau, Carolyn, Linde, Caitlin, Maddur, Mohan S., Das, Jishnu, Wang, Hong, Guthmiller, Jenna, Zheng, Nai-Ying, Huang, Min, Uphadhyay, Amit A., Gardinassi, Luiz, Petitdemange, Caroline, McCullough, Michele Paine, Johnson, Sara Jo, Gill, Kiran, Cervasi, Barbara, Zou, Jun, Bretin, Alexis, Hahn, Megan, Gewirtz, Andrew T., Bosinger, Steve E., Wilson, Patrick C., Li, Shuzhao, Alter, Galit, Khurana, Surender, Golding, Hana, and Pulendran, Bali

Published
2019
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5. Prevalence of the apolipoprotein E ε4 allele in amyloid β positive subjects across the spectrum of Alzheimer's disease

Author

Mattsson, Niklas, Groot, Colin, Jansen, Willemijn J., Landau, Susan M., Villemagne, Victor L., Engelborghs, Sebastiaan, Mintun, Mark M., Lleo, Alberto, Molinuevo, José Luis, Jagust, William J., Frisoni, Giovanni B., Ivanoiu, Adrian, Chételat, Gaël, Resende de Oliveira, Catarina, Rodrigue, Karen M., Kornhuber, Johannes, Wallin, Anders, Klimkowicz-Mrowiec, Aleksandra, Kandimalla, Ramesh, Popp, Julius, Aalten, Pauline P., Aarsland, Dag, Alcolea, Daniel, Almdahl, Ina S., Baldeiras, Inês, van Buchem, Mark A., Cavedo, Enrica, Chen, Kewei, Cohen, Ann D., Förster, Stefan, Fortea, Juan, Frederiksen, Kristian S., Freund-Levi, Yvonne, Gill, Kiran Dip, Gkatzima, Olymbia, Grimmer, Timo, Hampel, Harald, Herukka, Sanna-Kaisa, Johannsen, Peter, van Laere, Koen, de Leon, Mony J., Maier, Wolfgang, Marcusson, Jan, Meulenbroek, Olga, Møllergård, Hanne M., Morris, John C., Mroczko, Barbara, Nordlund, Arto, Prabhakar, Sudesh, Peters, Oliver, Rami, Lorena, Rodríguez-Rodríguez, Eloy, Roe, Catherine M., Rüther, Eckart, Santana, Isabel, Schröder, Johannes, Seo, Sang W., Soininen, Hilkka, Spiru, Luiza, Stomrud, Erik, Struyfs, Hanne, Teunissen, Charlotte E., Verhey, Frans R.J., Vos, Stephanie J.B., van Waalwijk van Doorn, Linda J.C., Waldemar, Gunhild, Wallin, Åsa K., Wiltfang, Jens, Vandenberghe, Rik, Brooks, David J., Fladby, Tormod, Rowe, Christopher C., Drzezga, Alexander, Verbeek, Marcel M., Sarazin, Marie, Wolk, David A., Fleisher, Adam S., Klunk, William E., Na, Duk L., Sánchez-Juan, Pascual, Lee, Dong Young, Nordberg, Agneta, Tsolaki, Magda, Camus, Vincent, Rinne, Juha O., Fagan, Anne M., Zetterberg, Henrik, Blennow, Kaj, Rabinovici, Gil D., Hansson, Oskar, van Berckel, Bart N.M., van der Flier, Wiesje M., Scheltens, Philip, Visser, Pieter Jelle, and Ossenkoppele, Rik

Published
2018
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16. Prevalence Estimates of Amyloid Abnormality Across the Alzheimer Disease Clinical Spectrum

Author

Jansen, Willemijn J, Janssen, Olin, von Arnim, Christine, Marquié, Marta, Martinez-Lage, Pablo, Maserejian, Nancy, Mattsson, Niklas, de Mendonça, Alexandre, Meyer, Philipp T, Miller, Bruce L, Minatani, Shinobu, Mintun, Mark A, Mok, Vincent C T, Baiardi, Simone, Molinuevo, Jose Luis, Morbelli, Silvia Daniela, Morris, John C, Mroczko, Barbara, Na, Duk L, Newberg, Andrew, Nobili, Flavio, Nordberg, Agneta, Olde Rikkert, Marcel G M, de Oliveira, Catarina Resende, Baldeiras, Ines, Olivieri, Pauline, Orellana, Adela, Paraskevas, George, Parchi, Piero, Pardini, Matteo, Parnetti, Lucilla, Peters, Oliver, Poirier, Judes, Popp, Julius, Prabhakar, Sudesh, Barthel, Henryk, Rabinovici, Gil D, Ramakers, Inez H, Rami, Lorena, Reiman, Eric M, Rinne, Juha O, Rodrigue, Karen M, Rodríguez-Rodriguez, Eloy, Roe, Catherine M, Rosa-Neto, Pedro, Rosen, Howard J, Bateman, Randall J, Rot, Uros, Rowe, Christopher C, Rüther, Eckart, Ruiz, Agustín, Sabri, Osama, Sakhardande, Jayant, Sánchez-Juan, Pascual, Sando, Sigrid Botne, Santana, Isabel, Sarazin, Marie, Van Berckel, Bart, Scheltens, Philip, Schröder, Johannes, Selnes, Per, Seo, Sang Won, Silva, Dina, Skoog, Ingmar, Snyder, Peter J, Soininen, Hilkka, Sollberger, Marc, Sperling, Reisa A, Binette, Alexa Pichet, Spiru, Luisa, Stern, Yaakov, Stomrud, Erik, Takeda, Akitoshi, Teichmann, Marc, Teunissen, Charlotte E, Thompson, Louisa I, Tomassen, Jori, Tsolaki, Magda, Vandenberghe, Rik, Blennow, Kaj, Verbeek, Marcel M, Verhey, Frans R J, Villemagne, Victor, Villeneuve, Sylvia, Vogelgsang, Jonathan, Waldemar, Gunhild, Wallin, Anders, Wallin, Åsa K, Wiltfang, Jens, Wolk, David A, Boada, Merce, Yen, Tzu-Chen, Zboch, Marzena, Zetterberg, Henrik, Boecker, Henning, Tijms, Betty M, Bottlaender, Michel, den Braber, Anouk, Brooks, David J, Van Buchem, Mark A, Camus, Vincent, Carill, Jose Manuel, Cerman, Jiri, Chen, Kewei, Chételat, Gaël, Chipi, Elena, Vos, Stephanie J B, Cohen, Ann D, Daniels, Alisha, Delarue, Marion, Didic, Mira, Drzezga, Alexander, Dubois, Bruno, Eckerström, Marie, Ekblad, Laura L, Engelborghs, Sebastiaan, Epelbaum, Stéphane, Ossenkoppele, Rik, Fagan, Anne M, Fan, Yong, Fladby, Tormod, Fleisher, Adam S, Van der Flier, Wiesje M, Förster, Stefan, Fortea, Juan, Frederiksen, Kristian Steen, Freund-Levi, Yvonne, Frings, Lars, Visser, Pieter Jelle, Frisoni, Giovanni B, Fröhlich, Lutz, Gabryelewicz, Tomasz, Gertz, Hermann-Josef, Gill, Kiran Dip, Gkatzima, Olymbia, Gómez-Tortosa, Estrella, Grimmer, Timo, Guedj, Eric, Habeck, Christian G, Group, Amyloid Biomarker Study, Hampel, Harald, Handels, Ron, Hansson, Oskar, Hausner, Lucrezia, Hellwig, Sabine, Heneka, Michael, Herukka, Sanna-Kaisa, Hildebrandt, Helmut, Hodges, John, Hort, Jakub, Aarsland, Dag, Huang, Chin-Chang, Iriondo, Ane Juaristi, Itoh, Yoshiaki, Ivanoiu, Adrian, Jagust, William J, Jessen, Frank, Johannsen, Peter, Johnson, Keith A, Kandimalla, Ramesh, Kapaki, Elisabeth N, Alcolea, Daniel, Kern, Silke, Kilander, Lena, Klimkowicz-Mrowiec, Aleksandra, Klunk, William E, Koglin, Norman, Kornhuber, Johannes, Kramberger, Milica G, Kuo, Hung-Chou, Van Laere, Koen, Landau, Susan M, Altomare, Daniele, Landeau, Brigitte, Lee, Dong Young, de Leon, Mony, Leyton, Cristian E, Lin, Kun-Ju, Lleó, Alberto, Löwenmark, Malin, Madsen, Karine, Maier, Wolfgang, Marcusson, Jan, Clinical sciences, Neuroprotection & Neuromodulation, Neurology, Amsterdam Neuroscience - Brain Imaging, Amsterdam Neuroscience - Neurodegeneration, Radiology and nuclear medicine, Laboratory Medicine, Amsterdam Neuroscience - Neuroinfection & -inflammation, APH - Personalized Medicine, APH - Methodology, RS: MHeNs - R1 - Cognitive Neuropsychiatry and Clinical Neuroscience, and Psychiatrie & Neuropsychologie

Subjects
Male, MILD COGNITIVE IMPAIRMENT, epidemiology [Cognitive Dysfunction], positron emission tomography, Alzheimer`s disease Donders Center for Medical Neuroscience [Radboudumc 1], epidemiology [Alzheimer Disease], Neuroscience(all), diagnostic imaging [Cognitive Dysfunction], Amyloidogenic Proteins, tau Proteins, cerebrospinal fluid [Amyloid beta-Peptides], DIAGNOSIS, cerebrospinal fluid, Apolipoproteins E, Alzheimer Disease, Prevalence, Humans, Amyloid, Alzheimer, PET, Cognitive Dysfunction, ddc:610, cerebrospinal fluid [Peptide Fragments], Aged, Amyloid beta-Peptides, neurology, DEMENTIA, Correction, ASSOCIATION, Amyloidosis, Middle Aged, Disorders of movement Donders Center for Medical Neuroscience [Radboudumc 3], health care planning, clinical trial design, Peptide Fragments, cerebrospinal fluid [Alzheimer Disease], PET, DRIFT, Cross-Sectional Studies, cerebrospinal fluid [Biomarkers], cerebrospinal fluid [tau Proteins], Radiology Nuclear Medicine and imaging, Positron-Emission Tomography, genetics [Apolipoproteins E], Female, Neurology (clinical), diagnostic imaging [Alzheimer Disease], cerebral amyloid aggregation, Biomarkers
Abstract

Importance: One characteristic histopathological event in Alzheimer disease (AD) is cerebral amyloid aggregation, which can be detected by biomarkers in cerebrospinal fluid (CSF) and on positron emission tomography (PET) scans. Prevalence estimates of amyloid pathology are important for health care planning and clinical trial design.Objective: To estimate the prevalence of amyloid abnormality in persons with normal cognition, subjective cognitive decline, mild cognitive impairment, or clinical AD dementia and to examine the potential implications of cutoff methods, biomarker modality (CSF or PET), age, sex, APOE genotype, educational level, geographical region, and dementia severity for these estimates.Design, Setting, and Participants: This cross-sectional, individual-participant pooled study included participants from 85 Amyloid Biomarker Study cohorts. Data collection was performed from January 1, 2013, to December 31, 2020. Participants had normal cognition, subjective cognitive decline, mild cognitive impairment, or clinical AD dementia. Normal cognition and subjective cognitive decline were defined by normal scores on cognitive tests, with the presence of cognitive complaints defining subjective cognitive decline. Mild cognitive impairment and clinical AD dementia were diagnosed according to published criteria.Exposures: Alzheimer disease biomarkers detected on PET or in CSF.Main Outcomes and Measures: Amyloid measurements were dichotomized as normal or abnormal using cohort-provided cutoffs for CSF or PET or by visual reading for PET. Adjusted data-driven cutoffs for abnormal amyloid were calculated using gaussian mixture modeling. Prevalence of amyloid abnormality was estimated according to age, sex, cognitive status, biomarker modality, APOE carrier status, educational level, geographical location, and dementia severity using generalized estimating equations.Results: Among the 19 097 participants (mean [SD] age, 69.1 [9.8] years; 10 148 women [53.1%]) included, 10 139 (53.1%) underwent an amyloid PET scan and 8958 (46.9%) had an amyloid CSF measurement. Using cohort-provided cutoffs, amyloid abnormality prevalences were similar to 2015 estimates for individuals without dementia and were similar across PET- and CSF-based estimates (24%; 95% CI, 21%-28%) in participants with normal cognition, 27% (95% CI, 21%-33%) in participants with subjective cognitive decline, and 51% (95% CI, 46%-56%) in participants with mild cognitive impairment, whereas for clinical AD dementia the estimates were higher for PET than CSF (87% vs 79%; mean difference, 8%; 95% CI, 0%-16%; P = .04). Gaussian mixture modeling-based cutoffs for amyloid measures on PET scans were similar to cohort-provided cutoffs and were not adjusted. Adjusted CSF cutoffs resulted in a 10% higher amyloid abnormality prevalence than PET-based estimates in persons with normal cognition (mean difference, 9%; 95% CI, 3%-15%; P = .004), subjective cognitive decline (9%; 95% CI, 3%-15%; P = .005), and mild cognitive impairment (10%; 95% CI, 3%-17%; P = .004), whereas the estimates were comparable in persons with clinical AD dementia (mean difference, 4%; 95% CI, -2% to 9%; P = .18).Conclusions and Relevance: This study found that CSF-based estimates using adjusted data-driven cutoffs were up to 10% higher than PET-based estimates in people without dementia, whereas the results were similar among people with dementia. This finding suggests that preclinical and prodromal AD may be more prevalent than previously estimated, which has important implications for clinical trial recruitment strategies and health care planning policies.

Published
2022
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20. Prevalence of Cerebral Amyloid Pathology in Persons Without Dementia: A Meta-analysis

Author

Jansen, Willemijn J., Ossenkoppele, Rik, Knol, Dirk L., Tijms, Betty M., Scheltens, Philip, Verhey, Frans R. J., Visser, Pieter Jelle, Aalten, Pauline, Aarsland, Dag, Alcolea, Daniel, Alexander, Myriam, Almdahl, Ina S., Arnold, Steven E., Baldeiras, Inês, Barthel, Henryk, van Berckel, Bart N. M., Bibeau, Kristen, Blennow, Kaj, Brooks, David J., van Buchem, Mark A., Camus, Vincent, Cavedo, Enrica, Chen, Kewei, Chetelat, Gael, Cohen, Ann D., Drzezga, Alexander, Engelborghs, Sebastiaan, Fagan, Anne M., Fladby, Tormod, Fleisher, Adam S., van der Flier, Wiesje M., Ford, Lisa, Förster, Stefan, Fortea, Juan, Foskett, Nadia, Frederiksen, Kristian S., Freund-Levi, Yvonne, Frisoni, Giovanni B., Froelich, Lutz, Gabryelewicz, Tomasz, Gill, Kiran Dip, Gkatzima, Olymbia, Gómez-Tortosa, Estrella, Gordon, Mark Forrest, Grimmer, Timo, Hampel, Harald, Hausner, Lucrezia, Hellwig, Sabine, Herukka, Sanna-Kaisa, Hildebrandt, Helmut, Ishihara, Lianna, Ivanoiu, Adrian, Jagust, William J., Johannsen, Peter, Kandimalla, Ramesh, Kapaki, Elisabeth, Klimkowicz-Mrowiec, Aleksandra, Klunk, William E., Köhler, Sebastian, Koglin, Norman, Kornhuber, Johannes, Kramberger, Milica G., Van Laere, Koen, Landau, Susan M., Lee, Dong Young, de Leon, Mony, Lisetti, Viviana, Lleó, Alberto, Madsen, Karine, Maier, Wolfgang, Marcusson, Jan, Mattsson, Niklas, de Mendonça, Alexandre, Meulenbroek, Olga, Meyer, Philipp T., Mintun, Mark A., Mok, Vincent, Molinuevo, José Luis, Møllergård, Hanne M., Morris, John C., Mroczko, Barbara, Van der Mussele, Stefan, Na, Duk L., Newberg, Andrew, Nordberg, Agneta, Nordlund, Arto, Novak, Gerald P., Paraskevas, George P., Parnetti, Lucilla, Perera, Gayan, Peters, Oliver, Popp, Julius, Prabhakar, Sudesh, Rabinovici, Gil D., Ramakers, Inez H. G. B., Rami, Lorena, Resende de Oliveira, Catarina, Rinne, Juha O., Rodrigue, Karen M., Rodríguez-Rodríguez, Eloy, Roe, Catherine M., Rot, Uros, Rowe, Christopher C., Rüther, Eckart, Sabri, Osama, Sanchez-Juan, Páscual, Santana, Isabel, Sarazin, Marie, Schröder, Johannes, Schütte, Christin, Seo, Sang W., Soetewey, Femke, Soininen, Hilkka, Spiru, Luiza, Struyfs, Hanne, Teunissen, Charlotte E., Tsolaki, Magda, Vandenberghe, Rik, Verbeek, Marcel M., Villemagne, Victor L., Vos, Stephanie J. B., van Waalwijk van Doorn, Linda J. C., Waldemar, Gunhild, Wallin, Anders, Wallin, Åsa K., Wiltfang, Jens, Wolk, David A., Zboch, Marzena, and Zetterberg, Henrik

Published
2015
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49. siRNA against presenilin 1 (PS1) down regulates amyloid β42 production in IMR-32 cells

Author

Kandimalla Ramesh JL, Wani Willayat, BK Binukumar, and Gill Kiran

Subjects
Alzheimer's Disease, presenilins, siRNA, Aβ42, IMR-32 Cells, Medicine
Abstract

Abstract Background One of the pathological hallmarks of Alzheimer's disease (AD) is the deposition of the ~4 kDa amyloid β protein (Aβ) within lesions known as senile plaques. Aβ is also deposited in the walls of cerebral blood vessels in many cases of AD. A substantial proportion of the Aβ that accumulates in the AD brain is deposited as Amyloid, which is highly insoluble, proteinaceous material with a β-pleated-sheet conformation and deposited extracellularly in the form of 5-10 nm wide straight fibrils. As γ-secretase catalyzes the final cleavage that releases the Aβ42 or 40 from amyloid β -protein precursor (APP), therefore, it is a potential therapeutic target for the treatment of AD. γ-Secretase cleavage is performed by a high molecular weight protein complex containing presenilins (PSs), nicastrin, Aph-1 and Pen-2. Previous studies have demonstrated that the presenilins (PS1 and PS2) are critical components of a large enzyme complex that performs γ-secretase cleavage. Methods In this study we used RNA interference (RNAi) technology to examine the effects of small-interfering RNA (siRNA) against PS1 on expression levels of PS1 and Aβ42 in IMR-32 Cells using RTPCR, western blotting and immunofluorescence techniques. Results The results of the present study showed down regulation of PS1 and Aβ42 in IMR32 cells transfected with siRNA against PS1. Conclusion Our results substantiate the concept that PS1 is involved in γ-secretase activity and provides the rationale for therapeutic strategies aimed at influencing Aβ42 production.

Published
2012
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50. Nigrostriatal neuronal death following chronic dichlorvos exposure: crosstalk between mitochondrial impairments, α synuclein aggregation, oxidative damage and behavioral changes

Author

BK Binukumar, Bal Amanjit, Kandimalla Ramesh JL, and Gill Kiran

Subjects
Neurology. Diseases of the nervous system, RC346-429
Abstract

Abstract Background In recent years, several lines of evidence have shown an increase in Parkinson's disease prevalence in rural environments where pesticides are heavily used. Although, the underlying mechanism for neuronal degeneration in sporadic PD remains unknown, mitochondrial dysfunction, oxidative stress and proteasomal dysfunction are proposed as contributing factors. In this study rats were chronically and continuously exposed to the pesticide, dichlorvos to identify the molecular mechanism of nigrostaital neuronal degeneration. Result Chronic dichlorvos exposure (2.50 mg/kg b.wt.s.c/daily for 12 weeks) caused nigrostriatal dopaminergic degeneration. The degenerative changes were accompanied by a loss of 60-80% of the nigral dopamine neurons and 60-70% reduction in striatal dopamine and tyrosine hydroxylase levels. Dichlorvos exposed animals also showed α -synuclein and ubiquitin positive inclusions along with swollen, dystrophic neurites and mitochondrial abnormalities like decreased complex I&IV activities, increased mitochondrial size, axonal degeneration and presence of electron dense perinuclear cytoplasmic inclusions in the substantia nigra of rats. These animals also showed evidence of oxidative stress, including increased mitochondrial ROS levels, decreased MnSOD activity and increased lipid peroxidation. Measurable impairments in neurobehavioral indices were also observed. Notable exacerbations in motor impairments, open field and catalepsy were also evident in dichlorvos exposed animals. Conclusion All these findings taken together indicate that chronic dichlorvos exposure may cause nigrostaital neurodegenaration and significant behavioral impairments.

Published
2010
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