Diet in treatment of autism spectrum disorders

Alam, Sabiha; Westmark, Cara J.; McCullagh, Elizabeth A.

doi:10.3389/fnins.2022.1031016

Cited by 12 publications

(4 citation statements)

References 146 publications

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“…FXS is caused by the deficiency or absence of fragile X messenger ribonucleoprotein (FMRP), an RNA-binding protein (RBP) with a prominent role in the regulation of a large number of mRNAs in the brain and periphery . Our prior research demonstrates that single-source, soy protein-based diets exacerbate seizures in mouse models of FXS, Alzheimer’s disease, and Down syndrome, agreeing with numerous reports studying the effects of diet on CNS function . Soy-based diets contain high levels of plant estrogens (phytoestrogens, isoflavones), which can mimic or antagonize natural estrogen activity and affect neuronal excitability relevant to infant development .…”

Section: Introductionsupporting

confidence: 84%

On-Tissue Spatial Proteomics Integrating MALDI-MS Imaging with Shotgun Proteomics Reveals Soy Consumption-Induced Protein Changes in a Fragile X Syndrome Mouse Model

Ma,

Yu,

Delafield

et al. 2023

ACS Chem. Neurosci.

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Fragile X syndrome (FXS), the leading cause of inherited intellectual disability and autism, is caused by the transcriptional silencing of the FMR1 gene, which encodes the fragile X messenger ribonucleoprotein (FMRP). FMRP interacts with numerous brain mRNAs that are involved in synaptic plasticity and implicated in autism spectrum disorders. Our published studies indicate that single-source, soy-based diets are associated with increased seizures and autism. Thus, there is an acute need for an unbiased protein marker identification in FXS in response to soy consumption. Herein, we present a spatial proteomics approach integrating mass spectrometry imaging with label-free proteomics in the FXS mouse model to map the spatial distribution and quantify levels of proteins in the hippocampus and hypothalamus brain regions. In total, 1250 unique peptides were spatially resolved, demonstrating the diverse array of peptidomes present in the tissue slices and the broad coverage of the strategy. A group of proteins that are known to be involved in glycolysis, synaptic transmission, and coexpression network analysis suggest a significant association between soy proteins and metabolic and synaptic processes in the Fmr1 KO brain. Ultimately, this spatial proteomics work represents a crucial step toward identifying potential candidate protein markers and novel therapeutic targets for FXS.

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Section: Introductionsupporting

confidence: 84%

On-Tissue Spatial Proteomics Integrating MALDI-MS Imaging with Shotgun Proteomics Reveals Soy Consumption-Induced Protein Changes in a Fragile X Syndrome Mouse Model

Ma,

Yu,

Delafield

et al. 2023

ACS Chem. Neurosci.

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“…1 Culminando em seletividade alimentar 3 , obesidade 13 e deficiências de macro e micronutrientes. 14 Algumas características podem ser observadas antes mesmo dos 2 anos de idade, como por exemplo a dificuldade de manter contato visual, aversão ao toque físico e ao contato com determinadas texturas, recusa alimentar, dificuldades de fala e atitudes e preferências restritas e repetitivas. 1 E a identificação precoce dos sinais característicos do transtorno é essencial, principalmente na existência de distúrbios de alimentação.…”

Section: Resultsunclassified

Implicações Dietéticas No Transtorno Do Espectro Autista

Fernandes Pinheiro,

Radech de Lima

2024

RIPS

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Introdução: o Transtorno do Espectro Autista (TEA) é uma disfunção neurológica que afeta o desenvolvimento de habilidades sociais, cognitivas e linguísticas. Um dos desafios enfrentados por crianças com TEA é a seletividade alimentar, o que pode resultar em deficiências nutricionais, problemas de crescimento e alterações de peso. A importância de uma alimentação adequada no manejo do TEA tem sido enfatizada por diversos autores, uma vez que uma dieta balanceada pode influenciar positivamente os sintomas e comportamentos associados ao transtorno, proporcionando uma melhor qualidade de vida aos pacientes. O acompanhamento nutricional especializado desempenha um papel fundamental nesse processo, garantindo que a dieta seja adaptada às necessidades individuais de cada criança com TEA. Objetivo: busca-se realizar uma revisão bibliográfica para identificar as alterações alimentares frequentemente observadas em crianças e adolescentes com TEA, bem como investigar as possíveis intervenções nutricionais que podem ser adotadas. Método: trata-se de uma revisão de literatura elaborada através de buscas realizadas em diversas bases de dados, durante o período de janeiro a junho de 2023. Sendo considerados artigos científicos publicados entre os anos de 2013 e 2023, nos idiomas português e inglês. Resultados: a pesquisa possibilitou observar um crescente número de estudos que relacionam a melhora dos sintomas do TEA com a utilização de estratégias que visam a melhora do comportamento alimentar, enfatizando a importância da continuidade pesquisas voltadas ao tema. Conclusão: conclui-se que, embora ainda não existam evidências sólidas para intervenções dietéticas específicas no TEA, é necessária a continuidade das pesquisas nessa área. Enquanto isso, o acompanhamento cuidadoso dos hábitos alimentares e o uso de abordagens baseadas em evidências, quando apropriado, podem ser recursos importantes para auxiliar no manejo nutricional de crianças com TEA.

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“…Our laboratory is interested in validating actigraphy and polysomnography as outcome measures that translate between mice and humans and in identifying dietary and pharmaceutical interventions for FXS. KD therapy has shown success in treating epilepsy, repetitive behavior, intellectual impairment, language dysfunction, and social skills, as well as in improving sleep, i.e., increasing REM sleep and reducing nighttime awakenings and daytime sleepiness [ 50 , 51 , 52 ]. Previously, we quantitated EEG sleep metrics in adult mice commencing KD therapy at weaning at P18 and did not find good correlation between sleep as assessed by EEG and activity levels assessed by actigraphy [ 4 , 43 ].…”

Section: Discussionmentioning

confidence: 99%

Adult Inception of Ketogenic Diet Therapy Increases Sleep during the Dark Cycle in C57BL/6J Wild Type and Fragile X Mice

Westmark,

Swietlik,

Runde

et al. 2024

IJMS

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Sleep problems are a significant phenotype in children with fragile X syndrome. Our prior work assessed sleep–wake cycles in Fmr1KO male mice and wild type (WT) littermate controls in response to ketogenic diet therapy where mice were treated from weaning (postnatal day 18) through study completion (5–6 months of age). A potentially confounding issue with commencing treatment during an active period of growth is the significant reduction in weight gain in response to the ketogenic diet. The aim here was to employ sleep electroencephalography (EEG) to assess sleep–wake cycles in mice in response to the Fmr1 genotype and a ketogenic diet, with treatment starting at postnatal day 95. EEG results were compared with prior sleep outcomes to determine if the later intervention was efficacious, as well as with published rest-activity patterns to determine if actigraphy is a viable surrogate for sleep EEG. The data replicated findings that Fmr1KO mice exhibit sleep–wake patterns similar to wild type littermates during the dark cycle when maintained on a control purified-ingredient diet but revealed a genotype-specific difference during hours 4–6 of the light cycle of the increased wake (decreased sleep and NREM) state in Fmr1KO mice. Treatment with a high-fat, low-carbohydrate ketogenic diet increased the percentage of NREM sleep in both wild type and Fmr1KO mice during the dark cycle. Differences in sleep microstructure (length of wake bouts) supported the altered sleep states in response to ketogenic diet. Commencing ketogenic diet treatment in adulthood resulted in a 15% (WT) and 8.6% (Fmr1KO) decrease in body weight after 28 days of treatment, but not the severe reduction in body weight associated with starting treatment at weaning. We conclude that the lack of evidence for improved sleep during the light cycle (mouse sleep time) in Fmr1KO mice in response to ketogenic diet therapy in two studies suggests that ketogenic diet may not be beneficial in treating sleep problems associated with fragile X and that actigraphy is not a reliable surrogate for sleep EEG in mice.

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Diet in treatment of autism spectrum disorders

Cited by 12 publications

References 146 publications

On-Tissue Spatial Proteomics Integrating MALDI-MS Imaging with Shotgun Proteomics Reveals Soy Consumption-Induced Protein Changes in a Fragile X Syndrome Mouse Model

On-Tissue Spatial Proteomics Integrating MALDI-MS Imaging with Shotgun Proteomics Reveals Soy Consumption-Induced Protein Changes in a Fragile X Syndrome Mouse Model

Implicações Dietéticas No Transtorno Do Espectro Autista

Adult Inception of Ketogenic Diet Therapy Increases Sleep during the Dark Cycle in C57BL/6J Wild Type and Fragile X Mice

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