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1. First International Conference on Unconventional Animal Models of Alzheimers Disease and Aging.

Author

Cogram, Patricia, Garduño, B, Ren, Bing, and Xu, Xiangmin

Subjects
Aging, Alzheimer’s disease, Chile, animal model, conference, degu, dog, marmoset, meeting report, Humans, Mice, Animals, Dogs, Alzheimer Disease, Octodon, Aging, Mice, Transgenic, Disease Models, Animal
Abstract

The first International Conference on Unconventional Animal Models of Alzheimers Disease and Aging (UAMAA) took place on December 13-16, 2023, in Santiago, Chile. The Alzheimers disease (AD) research field is currently in search for new and unconventional models that could hold greater translational potential than transgenic mouse models. Thus this UAMAA conference is timely and significant. The event consisted of 6 sessions with talks from 28 world-class scientists from all over the world. These animal models of interest include the degu (Octodon degu), the dog (Canis familiaris), and certain species of nonhuman primates that may better recapitulate neuropathology and cognitive impairments in human AD. Our conference has provided a formal forum to discuss and highlight new research directions, alternative animal models, and innovative approaches for the AD and aging research field.

Published
2024

2. How the forebrain transitions to adulthood: developmental plasticity markers in a long-lived rodent reveal region diversity and the uniqueness of adolescence.

Author

Garduño, B, Hanni, Patrick, Hays, Chelsea, Cogram, Patricia, Insel, Nathan, and Xu, Xiangmin

Subjects
adolescence, degu (Octodon degus), microglia, perineuronal net (PNN), plasticity
Abstract

Maturation of the forebrain involves transitions from higher to lower levels of synaptic plasticity. The timecourse of these changes likely differs between regions, with the stabilization of some networks scaffolding the development of others. To gain better insight into neuroplasticity changes associated with maturation to adulthood, we examined the distribution of two molecular markers for developmental plasticity. We conducted the examination on male and female degus (Octodon degus), a rodent species with a relatively long developmental timecourse that offers a promising model for studying both development and age-related neuropathology. Immunofluorescent staining was used to measure perineuronal nets (PNNs), an extracellular matrix structure that emerges during the closure of critical plasticity periods, as well as microglia, resident immune cells that play a crucial role in synapse remodeling during development. PNNs (putatively restricting plasticity) were found to be higher in non-juvenile (>3 month) degus, while levels of microglia (putatively mediating plasticity) decreased across ages more gradually, and with varying timecourses between regions. Degus also showed notable variation in PNN levels between cortical layers and hippocampal subdivisions that have not been previously reported in other species. These results offer a glimpse into neuroplasticity changes occurring during degu maturation and highlight adolescence as a unique phase of neuroplasticity, in which PNNs have been established but microglia remain relatively high.

Published
2024

5. Genome Sequencing Variations in the Octodon degus, an Unconventional Natural Model of Aging and Alzheimer's Disease

Author

Hurley, Michael J, Urra, Claudio, Garduno, B Maximiliano, Bruno, Agostino, Kimbell, Allison, Wilkinson, Brent, Marino-Buslje, Cristina, Ezquer, Marcelo, Ezquer, Fernando, Aburto, Pedro F, Poulin, Elie, Vasquez, Rodrigo A, Deacon, Robert, Avila, Ariel, Altimiras, Francisco, Vanderklish, Peter Whitney, Zampieri, Guido, Angione, Claudio, Constantino, Gabriele, Holmes, Todd C, Coba, Marcelo P, Xu, Xiangmin, and Cogram, Patricia

Subjects
Biological Psychology, Biomedical and Clinical Sciences, Neurosciences, Psychology, Alzheimer's Disease, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Neurodegenerative, Brain Disorders, Aging, Genetics, Human Genome, Acquired Cognitive Impairment, Dementia, Aetiology, 1.1 Normal biological development and functioning, 2.1 Biological and endogenous factors, Underpinning research, Neurological, Alzheimer's disease, aging, genome, APOE, amyloids, lipid droplets, Octodon degus, drug development, Biochemistry and Cell Biology, Cognitive Sciences, Biological psychology
Abstract

The degu (Octodon degus) is a diurnal long-lived rodent that can spontaneously develop molecular and behavioral changes that mirror those seen in human aging. With age some degu, but not all individuals, develop cognitive decline and brain pathology like that observed in Alzheimer's disease including neuroinflammation, hyperphosphorylated tau and amyloid plaques, together with other co-morbidities associated with aging such as macular degeneration, cataracts, alterations in circadian rhythm, diabetes and atherosclerosis. Here we report the whole-genome sequencing and analysis of the degu genome, which revealed unique features and molecular adaptations consistent with aging and Alzheimer's disease. We identified single nucleotide polymorphisms in genes associated with Alzheimer's disease including a novel apolipoprotein E (Apoe) gene variant that correlated with an increase in amyloid plaques in brain and modified the in silico predicted degu APOE protein structure and functionality. The reported genome of an unconventional long-lived animal model of aging and Alzheimer's disease offers the opportunity for understanding molecular pathways involved in aging and should help advance biomedical research into treatments for Alzheimer's disease.

Published
2022

6. Dementia in Latin America: Paving the way toward a regional action plan.

Author

Parra, Mario Alfredo, Baez, Sandra, Sedeño, Lucas, Gonzalez Campo, Cecilia, Santamaría-García, Hernando, Aprahamian, Ivan, Bertolucci, Paulo Hf, Bustin, Julian, Camargos Bicalho, Maria Aparecida, Cano-Gutierrez, Carlos, Caramelli, Paulo, Chaves, Marcia LF, Cogram, Patricia, Beber, Bárbara Costa, Court, Felipe A, de Souza, Leonardo Cruz, Custodio, Nilton, Damian, Andres, de la Cruz, Myriam, Diehl Rodriguez, Roberta, Brucki, Sonia Maria Dozzi, Fajersztajn, Lais, Farías, Gonzalo A, De Felice, Fernanda G, Ferrari, Raffaele, de Oliveira, Fabricio Ferreira, Ferreira, Sergio T, Ferretti, Ceres, Figueredo Balthazar, Marcio Luiz, Ferreira Frota, Norberto Anizio, Fuentes, Patricio, García, Adolfo M, Garcia, Patricia J, de Gobbi Porto, Fábio Henrique, Duque Peñailillo, Lissette, Engler, Henry Willy, Maier, Irene, Mata, Ignacio F, Gonzalez-Billault, Christian, Lopez, Oscar L, Morelli, Laura, Nitrini, Ricardo, Quiroz, Yakeel T, Guerrero Barragan, Alejandra, Huepe, David, Pio, Fabricio Joao, Suemoto, Claudia Kimie, Kochhann, Renata, Kochen, Silvia, Kumfor, Fiona, Lanata, Serggio, Miller, Bruce, Mansur, Leticia Lessa, Hosogi, Mirna Lie, Lillo, Patricia, Llibre Guerra, Jorge, Lira, David, Lopera, Francisco, Comas, Adelina, Avila-Funes, José Alberto, Sosa, Ana Luisa, Ramos, Claudia, Resende, Elisa de Paula França, Snyder, Heather M, Tarnanas, Ioannis, Yokoyama, Jenifer, Llibre, Juan, Cardona, Juan Felipe, Possin, Kate, Kosik, Kenneth S, Montesinos, Rosa, Moguilner, Sebastian, Solis, Patricia Cristina Lourdes, Ferretti-Rebustini, Renata Eloah de Lucena, Ramirez, Jeronimo Martin, Matallana, Diana, Mbakile-Mahlanza, Lingani, Marques Ton, Alyne Mendonça, Tavares, Ronnielly Melo, Miotto, Eliane C, Muniz-Terrera, Graciela, Muñoz-Nevárez, Luis Arnoldo, Orozco, David, Okada de Oliveira, Maira, Piguet, Olivier, Pintado Caipa, Maritza, Piña Escudero, Stefanie Danielle, Schilling, Lucas Porcello, Rodrigues Palmeira, André Luiz, Yassuda, Mônica Sanches, Santacruz-Escudero, Jose Manuel, Serafim, Rodrigo Bernardo, Smid, Jerusa, Slachevsky, Andrea, Serrano, Cecilia, Soto-Añari, Marcio, Takada, Leonel Tadao, Grinberg, Lea Tenenholz, Teixeira, Antonio Lucio, and Barbosa, Maira Tonidandel

Subjects
Latin America, biomarkers, clinical trials, dementia, epidemiology, evidence-based recommendations, genetics, knowledge to action framework, networking and translational research, nonpharmacological interventions, Dementia, Clinical Research, Brain Disorders, Aging, Acquired Cognitive Impairment, Prevention, Neurological, Clinical Sciences, Neurosciences, Geriatrics
Abstract

Across Latin American and Caribbean countries (LACs), the fight against dementia faces pressing challenges, such as heterogeneity, diversity, political instability, and socioeconomic disparities. These can be addressed more effectively in a collaborative setting that fosters open exchange of knowledge. In this work, the Latin American and Caribbean Consortium on Dementia (LAC-CD) proposes an agenda for integration to deliver a Knowledge to Action Framework (KtAF). First, we summarize evidence-based strategies (epidemiology, genetics, biomarkers, clinical trials, nonpharmacological interventions, networking, and translational research) and align them to current global strategies to translate regional knowledge into transformative actions. Then we characterize key sources of complexity (genetic isolates, admixture in populations, environmental factors, and barriers to effective interventions), map them to the above challenges, and provide the basic mosaics of knowledge toward a KtAF. Finally, we describe strategies supporting the knowledge creation stage that underpins the translational impact of KtAF.

Published
2021

10. Effects of the sigma-1 receptor agonist blarcamesine in a murine model of fragile X syndrome: neurobehavioral phenotypes and receptor occupancy

Author

Reyes, Samantha T., Deacon, Robert M. J., Guo, Scarlett G., Altimiras, Francisco J., Castillo, Jessa B., van der Wildt, Berend, Morales, Aimara P., Park, Jun Hyung, Klamer, Daniel, Rosenberg, Jarrett, Oberman, Lindsay M., Rebowe, Nell, Sprouse, Jeffrey, Missling, Christopher U., McCurdy, Christopher R., Cogram, Patricia, Kaufmann, Walter E., and Chin, Frederick T.

Published
2021
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14. Distribution of AGG interruption patterns within nine world populations

Author

Yrigollen, Carolyn M, Sweha, Stefan, Durbin-Johnson, Blythe, Zhou, Lili, Berry-Kravis, Elizabeth, Fernandez-Carvajal, Isabel, Faradz, Sultana Mh, Amiri, Khaled, Shaheen, Huda, Polli, Roberta, Murillo-Bonilla, Luis, Silva Arevalo, Gabriel de Jesus, Cogram, Patricia, Murgia, Alessandra, and Tassone, Flora

Subjects
Pediatric, Brain Disorders, Genetics, Rare Diseases, Intellectual and Developmental Disabilities (IDD), Clinical Research, Fragile X Syndrome, AGG interruptions, FMR1 allele, CGG repeat, expansion, ethnicity, Clinical Sciences, Pharmacology and Pharmaceutical Sciences
Abstract

The CGG trinucleotide repeat within the FMR1 gene is associated with multiple clinical disorders, including fragile X-associated tremor/ataxia syndrome, fragile X-associated primary ovarian insufficiency, and fragile X syndrome. Differences in the distribution and prevalence of CGG repeat length and of AGG interruption patterns have been reported among different populations and ethnicities. In this study we characterized the AGG interruption patterns within 3,065 normal CGG repeat alleles from nine world populations including Australia, Chile, United Arab Emirates, Guatemala, Indonesia, Italy, Mexico, Spain, and United States. Additionally, we compared these populations with those previously reported, and summarized the similarities and differences. We observed significant differences in AGG interruption patterns. Frequencies of longer alleles, longer uninterrupted CGG repeat segments and alleles with greater than 2 AGG interruptions varied between cohorts. The prevalence of fragile X syndrome and FMR1 associated disorders in various populations is thought to be affected by the total length of the CGG repeat and may also be influenced by the AGG distribution pattern. Thus, the results of this study may be important in considering the risk of fragile X-related conditions in various populations.

Published
2014

15. Inositol and protein kinase C in the prevention of neural tube defects

Author

Cogram, Patricia

Subjects
612.8
Abstract

A number of mouse genetic mutants develop neural tube defects (NTDs). In some cases, defects can be prevented by administration of folic acid during pregnancy, whereas in other mutants there is no response. This parallels the human situation in which a proportion of NTDs appear resistant to folic acid therapy. Curly tail is the best characterised mouse model of folic acid-resistant NTDs. Previously it was shown that the incidence of spina bifida in curly tail mice can be reduced by administration of inositol during embryonic development. In this thesis, I compared the effectiveness of two isomers, myo- and D-chiro-inositol, with administration either directly to embryos in vitro, or to pregnant females by subcutaneous or oral routes. Although both inositols exerted a preventive effect on spina bifida, by all routes of administration, D-chiro-inositol consistently exhibited greater potency than myo-inositol. The protective effect of inositol has been shown previously to be mediated through the activity of the inositol/lipid cycle and to depend on downstream activation of protein kinase C (PKC). In the studies decscribed in this thesis, I examined the role of PKC in more detail. The expression of PKC isoforms was first examined by irrmiunohistochemistry, Broad spectrum chemical inhibitors were then used in whole embryo culture to confirm that one or more PKC isoforms are indispensable for normalisation of neural tube closure by inositol. Specific peptide inhibitors were then applied, and revealed that PKC beta I, gamma and zeta are most important in the protective pathway. Finally, I demonstrated that inositol stimulates cell proliferation in the hindgut of curly tail embryos, reversing the imbalance of cell proliferation that is known to lead, via enhanced ventral curvature of the caudal region, to delay or failure of neural tube closure.

Published
2008

17. The inhibition of NCS-1 binding to Ric8a rescues fragile X syndrome mice model phenotypes

Author

Fundación la Caixa, National Fragile X Foundation, Ministerio de Ciencia e Innovación (España), Instituto de Salud Carlos III, Cogram, Patricia [0000-0002-4198-0821], Fernández-Beltrán, Luis C. [0000-0001-6086-8301], Casarejos, María José [0000-0003-1288-1717], García-Rubia, Alfonso [0000-0003-4002-910X], Sánchez-Barrena, María José [0000-0002-5986-1804], Gil, Carmen [0000-0002-3882-6081], Martínez, Ana [0000-0002-2707-8110], Mansilla, Alicia [0000-0002-2192-5112], Cogram, Patricia, Fernández-Beltrán, Luis C., Casarejos, María José, Sánchez-Yepes, Sonia, Rodríguez-Martín, Eulalia, García-Rubia, Alfonso, Sánchez-Barrena, María José, Gil, Carmen, Martínez Gil, Ana, Mansilla, Alicia, Fundación la Caixa, National Fragile X Foundation, Ministerio de Ciencia e Innovación (España), Instituto de Salud Carlos III, Cogram, Patricia [0000-0002-4198-0821], Fernández-Beltrán, Luis C. [0000-0001-6086-8301], Casarejos, María José [0000-0003-1288-1717], García-Rubia, Alfonso [0000-0003-4002-910X], Sánchez-Barrena, María José [0000-0002-5986-1804], Gil, Carmen [0000-0002-3882-6081], Martínez, Ana [0000-0002-2707-8110], Mansilla, Alicia [0000-0002-2192-5112], Cogram, Patricia, Fernández-Beltrán, Luis C., Casarejos, María José, Sánchez-Yepes, Sonia, Rodríguez-Martín, Eulalia, García-Rubia, Alfonso, Sánchez-Barrena, María José, Gil, Carmen, Martínez Gil, Ana, and Mansilla, Alicia

Abstract

Fragile X syndrome (FXS) is caused by the loss of function of Fragile X mental retardation protein (FMRP). FXS is one of the leading monogenic causes of intellectual disability (ID) and autism. Although it is caused by the failure of a single gene, FMRP that functions as an RNA binding protein affects a large number of genes secondarily. All these genes represent hundreds of potential targets and different mechanisms that account for multiple pathological features, thereby hampering the search for effective treatments. In this scenario, it seems desirable to reorient therapies toward more general approaches. Neuronal calcium sensor 1 (NCS-1), through its interaction with the guanine-exchange factor Ric8a, regulates the number of synapses and the probability of the release of a neurotransmitter, the two neuronal features that are altered in FXS and other neurodevelopmental disorders. Inhibitors of the NCS-1/Ric8a complex have been shown to be effective in restoring abnormally high synapse numbers as well as improving associative learning in FMRP mutant flies. Here, we demonstrate that phenothiazine FD44, an NCS-1/Ric8a inhibitor, has strong inhibition ability in situ and sufficient bioavailability in the mouse brain. More importantly, administration of FD44 to two different FXS mouse models restores well-known FXS phenotypes, such as hyperactivity, associative learning, aggressive behavior, stereotype, or impaired social approach. It has been suggested that dopamine (DA) may play a relevant role in the behavior and in neurodevelopmental disorders in general. We have measured DA and its metabolites in different brain regions, finding a higher metabolic rate in the limbic area, which is also restored with FD44 treatment. Therefore, in addition to confirming that the NCS-1/Ric8a complex is an excellent therapeutic target, we demonstrate the rescue effect of its inhibitor on the behavior of cognitive and autistic FXS mice and show DA metabolism as a FXS biochemical disea

Published
2022

21. Alteration of Fatty Acid Profile in Fragile X Syndrome

Author

Abolghasemi, Armita, primary, Carullo, Maria Paulina, additional, Aguilera, Ester Cisneros, additional, Laroui, Asma, additional, Plantefeve, Rosalie, additional, Rojas, Daniela, additional, Benachenhou, Serine, additional, Ramírez, María Victoria, additional, Proteau-Lemieux, Mélodie, additional, Lepage, Jean-François, additional, Corbin, François, additional, Plourde, Mélanie, additional, Farez, Mauricio, additional, Cogram, Patricia, additional, and Çaku, Artuela, additional

Published
2022
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24. Genome Sequencing Variations in the Octodon degus, an Unconventional Natural Model of Aging and Alzheimer's Disease

Author

Hurley, Michael J., primary, Urra, Claudio, additional, Garduno, B. Maximiliano, additional, Bruno, Agostino, additional, Kimbell, Allison, additional, Wilkinson, Brent, additional, Marino-Buslje, Cristina, additional, Ezquer, Marcelo, additional, Ezquer, Fernando, additional, Aburto, Pedro F., additional, Poulin, Elie, additional, Vasquez, Rodrigo A., additional, Deacon, Robert, additional, Avila, Ariel, additional, Altimiras, Francisco, additional, Whitney-Vanderklish, Peter, additional, Zampieri, Guido, additional, Angione, Claudio, additional, Constantino, Gabriele, additional, Holmes, Todd C., additional, Coba, Marcelo P., additional, Xu, Xiangmin, additional, and Cogram, Patricia, additional

Published
2022
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28. Effects of the Sigma-1 Receptor Agonist Blarcamesine in a Murine Model of Fragile X Syndrome: Neurobehavioral Phenotypes and Receptor Occupancy

Author

Reyes, Samantha T., primary, Deacon, Robert M.J., additional, Guo, Scarlett G., additional, Castillo, Jessa B., additional, Wildt, Berend van der, additional, Morales, Aimara P., additional, Park, Jun Hyung, additional, Klamer, Daniel, additional, Rosenberg, Jarrett, additional, Oberman, Lindsay M., additional, Rebowe, Nell, additional, Sprouse, Jeffrey, additional, Missling, Christopher U., additional, Cogram, Patricia, additional, Kaufmann, Walter E., additional, Chin, Frederick T., additional, McCurdy, Christopher R., additional, and Altimiras, Francisco J., additional

Published
2021
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30. Dementia in Latin America: Paving the way toward a regional action plan

Author

Parra, Mario Alfredo, primary, Baez, Sandra, additional, Sedeño, Lucas, additional, Gonzalez Campo, Cecilia, additional, Santamaría‐García, Hernando, additional, Aprahamian, Ivan, additional, Bertolucci, Paulo HF, additional, Bustin, Julian, additional, Camargos Bicalho, Maria Aparecida, additional, Cano‐Gutierrez, Carlos, additional, Caramelli, Paulo, additional, Chaves, Marcia L. F., additional, Cogram, Patricia, additional, Beber, Bárbara Costa, additional, Court, Felipe A., additional, de Souza, Leonardo Cruz, additional, Custodio, Nilton, additional, Damian, Andres, additional, de la Cruz, Myriam, additional, Diehl Rodriguez, Roberta, additional, Brucki, Sonia Maria Dozzi, additional, Fajersztajn, Lais, additional, Farías, Gonzalo A., additional, De Felice, Fernanda G., additional, Ferrari, Raffaele, additional, de Oliveira, Fabricio Ferreira, additional, Ferreira, Sergio T., additional, Ferretti, Ceres, additional, Figueredo Balthazar, Marcio Luiz, additional, Ferreira Frota, Norberto Anizio, additional, Fuentes, Patricio, additional, García, Adolfo M., additional, Garcia, Patricia J., additional, de Gobbi Porto, Fábio Henrique, additional, Duque Peñailillo, Lissette, additional, Engler, Henry Willy, additional, Maier, Irene, additional, Mata, Ignacio F., additional, Gonzalez‐Billault, Christian, additional, Lopez, Oscar L., additional, Morelli, Laura, additional, Nitrini, Ricardo, additional, Quiroz, Yakeel T., additional, Guerrero Barragan, Alejandra, additional, Huepe, David, additional, Pio, Fabricio Joao, additional, Suemoto, Claudia Kimie, additional, Kochhann, Renata, additional, Kochen, Silvia, additional, Kumfor, Fiona, additional, Lanata, Serggio, additional, Miller, Bruce, additional, Mansur, Leticia Lessa, additional, Hosogi, Mirna Lie, additional, Lillo, Patricia, additional, Llibre Guerra, Jorge, additional, Lira, David, additional, Lopera, Francisco, additional, Comas, Adelina, additional, Avila‐Funes, José Alberto, additional, Sosa, Ana Luisa, additional, Ramos, Claudia, additional, Resende, Elisa de Paula França, additional, Snyder, Heather M., additional, Tarnanas, Ioannis, additional, Yokoyama, Jenifer, additional, Llibre, Juan, additional, Cardona, Juan Felipe, additional, Possin, Kate, additional, Kosik, Kenneth S., additional, Montesinos, Rosa, additional, Moguilner, Sebastian, additional, Solis, Patricia Cristina Lourdes, additional, Ferretti‐Rebustini, Renata Eloah de Lucena, additional, Ramirez, Jeronimo Martin, additional, Matallana, Diana, additional, Mbakile‐Mahlanza, Lingani, additional, Marques Ton, Alyne Mendonça, additional, Tavares, Ronnielly Melo, additional, Miotto, Eliane C, additional, Muniz‐Terrera, Graciela, additional, Muñoz‐Nevárez, Luis Arnoldo, additional, Orozco, David, additional, Okada de Oliveira, Maira, additional, Piguet, Olivier, additional, Pintado Caipa, Maritza, additional, Piña Escudero, Stefanie Danielle, additional, Schilling, Lucas Porcello, additional, Rodrigues Palmeira, André Luiz, additional, Yassuda, Mônica Sanches, additional, Santacruz‐Escudero, Jose Manuel, additional, Serafim, Rodrigo Bernardo, additional, Smid, Jerusa, additional, Slachevsky, Andrea, additional, Serrano, Cecilia, additional, Soto‐Añari, Marcio, additional, Takada, Leonel Tadao, additional, Grinberg, Lea Tenenholz, additional, Teixeira, Antonio Lucio, additional, Barbosa, Maira Tonidandel, additional, Trépel, Dominic, additional, and Ibanez, Agustin, additional

Published
2020
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32. Reversal of behavioural phenotype by the cannabinoid-like compound VSN16R in fragile X syndrome mice.

Author

Hurley, Michael J, Deacon, Robert M J, Chan, A W Edith, Baker, David, Selwood, David L, and Cogram, Patricia

Subjects
NERVE tissue proteins, ANIMAL experimentation, HYDROCARBONS, FRAGILE X syndrome, RESEARCH funding, MICE, PHENOTYPES
Abstract

Fragile X syndrome is the most common inherited intellectual disability and mono-genetic cause of autism spectrum disorder. It is a neurodevelopmental condition occurring due to a CGG trinucleotide expansion in the FMR1 gene. Polymorphisms and variants in large-conductance calcium-activated potassium channels are increasingly linked to intellectual disability and loss of FMR protein causes reduced large-conductance calcium-activated potassium channel activity leading to abnormalities in synapse function. Using the cannabinoid-like large-conductance calcium-activated potassium channel activator VSN16R we rescued behavioural deficits such as repetitive behaviour, hippocampal dependent tests of daily living, hyperactivity and memory in a mouse model of fragile X syndrome. VSN16R has been shown to be safe in a phase 1 study in healthy volunteers and in a phase 2 study in patients with multiple sclerosis with high oral bioavailability and no serious adverse effects reported. VSN16R could therefore be directly utilized in a fragile X syndrome clinical study. Moreover, VSN16R showed no evidence of tolerance, which strongly suggests that chronic VSN16R may have great therapeutic value for fragile X syndrome and autism spectrum disorder. This study provides new insight into the pathophysiology of fragile X syndrome and identifies a new pathway for drug intervention for this debilitating disorder. [ABSTRACT FROM AUTHOR]

Published
2022
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36. Dementia in Latin America

Author

Parra, Mario A., Baez, Sandra, Allegri, Ricardo, Nitrini, Ricardo, Lopera, Francisco, Slachevsky, Andrea, Custodio, Nilton, Lira, David, Piguet, Olivier, Kumfor, Fiona, Huepe, David, Cogram, Patricia, Bak, Thomas, Manes, Facundo, Ibanez, Agustin, and Publica

Subjects
Views & Reviews, Latin America, Socioeconomic Factors, Research, Humans, Dementia, Public Health
Abstract

The demographic structure of Latin American countries (LAC) is fast approaching that of developing countries, and the predicted prevalence of dementia in the former already exceeds the latter. Dementia has been declared a global challenge, yet regions around the world show differences in both the nature and magnitude of such a challenge. This article provides evidence and insights on barriers which, if overcome, would enable the harmonization of strategies to tackle the dementia challenge in LAC. First, we analyze the lack of available epidemiologic data, the need for standardizing clinical practice and improving physician training, and the existing barriers regarding resources, culture, and stigmas. We discuss how these are preventing timely care and research. Regarding specific health actions, most LAC have minimal mental health facilities and do not have specific mental health policies or budgets specific to dementia. In addition, local regulations may need to consider the regional context when developing treatment and prevention strategies. The support needed nationally and internationally to enable a smooth and timely transition of LAC to a position that integrates global strategies is highlighted. We focus on shared issues of poverty, cultural barriers, and socioeconomic vulnerability. We identify avenues for collaboration aimed to study unique populations, improve valid assessment methods, and generate opportunities for translational research, thus establishing a regional network. The issues identified here point to future specific actions aimed at tackling the dementia challenge in LAC.

Published
2018

42. Brain Transcriptome Sequencing of a Natural Model of Alzheimer's Disease

Author

Altimiras, Francisco, primary, Uszczynska-Ratajczak, Barbara, additional, Camara, Francisco, additional, Vlasova, Anna, additional, Palumbo, Emilio, additional, Newhouse, Stephen, additional, Deacon, Robert M. J., additional, Farias, Leandro A. E., additional, Hurley, Michael J., additional, Loyola, David E., additional, Vásquez, Rodrigo A., additional, Dobson, Richard, additional, Guigó, Roderic, additional, and Cogram, Patricia, additional

Published
2017
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43. Natural AD-Like Neuropathology in Octodon degus: Impaired Burrowing and Neuroinflammation

Author

Deacon, Robert, primary, Altimiras, Francisco, additional, Bazan-Leon, Enrique, additional, Pyarasani, Rhada, additional, Nachtigall, Fabiane, additional, Santos, Leonardo, additional, Tsolaki, Anthony, additional, Pednekar, Lina, additional, Kishore, Uday, additional, Biekofsky, Rodolfo, additional, Vasquez, Rodrigo, additional, and Cogram, Patricia, additional

Published
2015
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45. Neurulation and Neural Tube Closure Defects

Author

Copp, Andrew, primary, Cogram, Patricia, additional, Fleming, Angeleen, additional, Gerrelli, Dianne, additional, Henderson, Deborah, additional, Hynes, Andrew, additional, Kolatsi-Joannou, Maria, additional, Murdoch, Jennifer, additional, and Ybot-Gonzalez, Patricia, additional

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46. Sonic hedgehog and the molecular regulation of mouse neural tube closure

Author

Wellcome Trust, Ybot, Patricia, Cogram, Patricia, Gerrelli, Dianne, Copp, Andrew J., Wellcome Trust, Ybot, Patricia, Cogram, Patricia, Gerrelli, Dianne, and Copp, Andrew J.

Abstract

Neural tube closure is a fundamental embryonic event whose molecular regulation is poorly understood. As mouse neurulation progresses along the spinal axis, there is a shift from midline neural plate bending to dorsolateral bending. Here, we show that midline bending is not essential for spinal closure since, in its absence, the neural tube can close by a 'default' mechanism involving dorsolateral bending, even at upper spinal levels. Midline and dorsolateral bending are regulated by mutually antagonistic signals from the notochord and surface ectoderm. Notochordal signaling induces midline bending and simultaneously inhibits dorsolateral bending. Sonic hedgehog is both necessary and sufficient to inhibit dorsolateral bending, but is neither necessary nor sufficient to induce midline bending, which seems likely to be regulated by another notochordal factor. Attachment of surface ectoderm cells to the neural plate is required for dorsolateral bending, which ensures neural tube closure in the absence of sonic hedgehog signaling.

Published
2002

47. Neurulation and neural tube closure defects

Author

Copp, Andrew J., Cogram, Patricia, Fleming, A., Gerrelli, D., Henderson, Deborah J., Hynes, A., Kolatsi-Joannou, M., Murdoch, J, Ybot, Patricia, Copp, Andrew J., Cogram, Patricia, Fleming, A., Gerrelli, D., Henderson, Deborah J., Hynes, A., Kolatsi-Joannou, M., Murdoch, J, and Ybot, Patricia

Abstract

The purpose of this chapter is to summarize some technical approaches and aspects of interpretation that are important when studying the process of neurulation and the origin of neural tube defects in mouse embryos. The techniques are not exclusive to studies of neurulation, so few protocols are described in practical detail. Instead, we emphasize the overall type of approach that appears most effective and give tips on the best application of standard techniques such as those described elsewhere in this and other volumes.

Published
2000

50. Neurulation and Neural Tube Closure Defects.

Author

Walker, John M., Tuan, Rocky S., Lo, Cecilia W., Copp, Andrew, Cogram, Patricia, Fleming, Angeleen, Gerrelli, Dianne, Henderson, Deborah, Hynes, Andrew, Kolatsi-Joannou, Maria, Murdoch, Jennifer, and Ybot-Gonzalez, Patricia

Abstract

The purpose of this chapter is to summarize some technical approaches and aspects of interpretation that are important when studying the process of neurulation and the origin of neural tube defects in mouse embryos. The techniques are not exclusive to studies of neurulation, so few protocols are described in practical detail. Instead, we emphasize the overall type of approach that appears most effective and give tips on the best application of standard techniques such as those described elsewhere in this and other volumes. [ABSTRACT FROM AUTHOR]

Published
2000
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