Huntington's disease

This experiment investigated the effects of verbal labels on recognition memory for ambiguous visual figures in patients with Alzheimer's disease (AD), patients with Huntington's disease (HD), and matched normal control subjects. The study employed ambiguous figures that could be interpreted in two different ways. During the study phase each figure was presented together with a verbal label that corresponded to one interpretation of the figure. After a 30-min retention interval a recognition memory test was given during which the study figures and distractor figures were presented one at a time without verbal labels. For each study figure two distractor figures were employed, each corresponding to a different interpretation of the study figure. The patients' overall recognition memory performance was severely impaired compared to control subjects. However, all subject groups tended to produce responses and response latencies to distractor items that were consistent with the verbal labels presented during the study phase. This bias effect occurred in the AD patients despite the fact that their recognition memory performance was at chance level. Indeed, there was no significant difference in the bias evidenced by the AD and HD patients and their respective matched control subjects. The bias effects were obtained in an explicit memory' task, and the findings are discussed in terms of unconscious influences on explicit memory processes.

Background: While it has been shown that aerobic exercise interventions are well tolerated in participants with the Huntington disease (HD) gene mutation, no study to date has tested whether an aerobic exercise intervention benefits brain structure and function in pre-manifest HD.

A Doença de Huntington é uma doença neurodegenerativa progressiva e que tem transmissão autossômica dominante do gene da "Huntingtina", proteína gerada por uma repetição aumentada da trinca de nucleotídeos CAG (citosina, adenosina e guanina), sendo o normal para o indivíduo saudável a ocorrência de 10 a 35 unidades desta (MIGUEL et al., 2012). Os sintomas da doença são basicamente, alterações cognitivas, em que o paciente torna-se progressivamente incapaz de resolver problemas e manter uma linha de conversação até que se chegue futuramente a ter demência; alterações de humor; comprometimento da marcha, onde o movimento voluntário torna-se difícil e lento, e a parte involuntária gera espasmos súbitos e arrítmicos chamados de "coreia" (do grego "dança"). (GIL-MOHAPEL, 2011) Geralmente ocorrem ainda perturbações psiquiátricas, como apatia e/ou depressão. Por ser neurodegenerativa, a Doença de Huntington, assim como as outras doenças deste tipo não possui cura ainda nos dias atuais, mas existem terapias medicamentosas que servem para retardar ou amenizar os sintomas causadores que devem ser estudadas para que se haja sempre um aprimoramento do tratamento para melhoria da qualidade de vida do paciente. (ROSENBLATT et al., 2006). Descrição da doença A Doença de Huntington é um distúrbio neurodegenerativo progressivo, que se torna fatal com o passar dos anos e que não tem cura. Esta doença é causada por uma mutação autossômica dominante (e por isso, existe teoricamente uma chance de 50% de um filho de uma pessoa heterozigota herdar o gene) nas repetições expandidas e instáveis da trinca CAG na região de codificação, ou exônica, 5′ do gene IT15 (Interesting Transcript15) localizado no cromossomo 4. Essa mutação gera uma proteína defeituosa, porém funcional, nomeada "Huntingtina" (MARTELLI, 2014). A quantidade de repetições desta trinca de CAG é o que determina o tempo e a agressividade de manifestação da doença. De acordo com as normas e diretrizes técnicas para testes de Doença de Huntington, alelos com 26 ou menos repetições de CAG nunca foram associados com fenótipo da doença. Alelos que contém entre 27 e 35 repetições CAG são raros e não foram convincentemente associados com fenótipo DH. Entretanto, alelos que contém entre 36 e 39 repetições de CAG foram Perspective

Huntington hastalığı, istemsiz koreik hareketler, bilişsel kayıplar ve psikolojik bozukluklarla karakterize edilen, otozomal dominant geçişli, geç başlangıçlı ve ölümcül bir hastalıktır. Hastalığa sebep olan mutasyon, IT-15 geninin birinci ek sonunda tekrar eden CAG bazlarının sayılarındaki artıştır. Mutant genin ifadesi, striyatal gam ma amino bütirik asit ile ten (GA BA-er jik) orta boy dikensi nö ronların seçimli ölümüne neden olur. Mutant huntingtin (htt) proteininin konformasyonu,
pro te in yı kı mı ve übi kü tin-pro te o zom sis te mi (UPS), gen ya zı lı mı dü zen le me le rin de ki de ği şim ler
ve ek si to tok si si te, nö ro de je ne ras yo nun mo le kü ler me ka niz ma la rı ara sın da dır. Uya rı cı kim ya sal la -
rın aşı rı mik ta rı hüc re le ri sü rek li uya ra rak has sas hüc re le rin ek si to tok sik ölüm le ri ne se bep olur lar.
Glu ta mat da ba zal gang li ya dan sa lı nan uya rı cı nö rot rans mi ter ler den bi ri dir. Hun ting ton has ta lı -
ğın da stri ya tal nö ron la rın kay be dil me si glu ta mat re sep tö rü ara cı lı ek si to tok si si te nin pa to ge nez de etki
li ola bi le ce ği ne işa ret eder. İyo not ro fik glu ta mat re sep tör le ri (iG luR) ara sın dan bi ri olan
N-me til-D-As par tat re sep tör le ri (NMDAR)’nin uya rıl ma sı ve bu nu ta ki ben nük le er fak tör kap pa B
(NF ± B) ya zı lım fak tö rü nün ak ti vas yo nu nö ro nal ölüm ile so nuç la nır. NMDAR, glu ta mat bağ lan -
ma böl ge le ri ne ek ola rak po li a min bağ lan ma böl ge le ri de içe rir. Po li a min le rin mu tant htt pro te i -
ni nin, NMDAR ve NF ± B ya zı lım fak tö rü ile ay rı ay rı iliş ki içe ri sin de ol ma sı, bu pro te i nin,
Hun ting ton has ta lı ğın da mey da na ge len nö ro de je ne ras yon da mer ke zi bir rol oy na ya bi le ce ği ni düşün
dür mek te dir. Bu ne den le, Hun ting ton has ta lı ğın da po li a min me ta bo liz ma sı nın de tay lı araş tırıl ma sı ve an la şıl ma sı has ta lı ğın te da vi sin de ye ni yak la şım lar üre til me si ni sağ la ya cak tır.

Among the several main reasons for the present gradual demise of the hitherto dominant hypotheses of 'modern' human origins, the replacement or 'out of Africa' models, are the issues of genetic drift and introgression. The operation and consequences of genetic drift are considered, especially in terms of their effects on the evolution of the human species during the Late Pleistocene period. The complexity of the subject is reviewed in the light of several relevant frames of reference, such as those provided by niche construction, gene-culture co-evolutionary theories, and by the domestication hypothesis. The current cultural, genetic and paleoanthropological evidence is reviewed, as well as other germane factors, such as the role of neurodegenerative pathologies, the neotenization of humans in their most recent evolutionary history, and the question of cultural selection-based self-domestication. This comprehensive review leads to a paradigmatic shift in the way recent human evolution needs to be viewed. This article explains fully how humans became what they are today.

Approximately 44 million people around the world already have Alzheimer’s disease and other forms of dementia. It’s the fastest-growing cause of death in the world.

Alzheimer’s disease is a member of an aggressive family of neurodegenerative diseases known as Transmissible Spongiform Encephalopathy (TSE). The operative word is “transmissible.” Related diseases are killing wildlife and livestock. The TSE epidemic represents an environmental nightmare that threatens every mammal on Earth.

TSEs include Alzheimer’s disease, Creutzfeldt-Jakob disease, Huntington’s disease, and Parkinson’s disease. TSEs also include mad cow disease and chronic wasting disease in deer. Few, if any, mammals are immune. There is no cure and there is no species barrier.

TSEs are caused by a deadly protein called a prion (PREE-on). Prion disease is unstoppable and the pathogen spreads through bodily fluids and cell tissue. Prions linger in the environment, homes, hospitals, nursing homes, dental offices, restaurants and many other places infinitely. They migrate, mutate, multiply and kill with unparalleled efficiency. Prions defy all attempts at sterilization and inactivation. Victims of the disease can spread the disease even further via bodily fluids and cell tissue. Victims often are contagious long before they appear sick.

This paper examines the songs that Woody Guthrie recorded for children and critiques the widely-perceived notion that they are simple and particularly childlike. The songs reveal much about Guthrie’s ethos of childhood, his views on fatherhood and his attitude to his burgeoning iconic status. As such they provide a valuable insight into his craft and his creativity. I examine the enduring link between folk music and Romantic discourses of childhood, both being informed by notions of simplicity and innocence. The paper highlights the unique circumstances of Guthrie’s compositions (many were written by and with his three-year-old daughter) and challenges claims made by Jacqueline Rose (1984) about the ‘impossibility’ of children’s culture. An analysis of Guthrie’s use of nonsense language and his adoption of children as narrators reveals his particular ideology of childhood. Rather than documenting innocent, asexual perma-children ‘fixed’ by the desire of adults in a lost ‘Neverland’ of childhood, Woody’s songs for children simmer with a worldliness that frames both him, daughter Cathy Ann and other ‘real-life’ children in the messy, sexualised age-shared experiences of everyday life. I examine the process by which two of Guthrie’s best-known children’s songs, ‘Put your finger in the air’ and ‘Riding in my car (Car song)’, have been transformed and simplified by subsequent artists, a process which I argue increases their childness (Hollindale, 1997) whilst ensuring their popularity and longevity. Finally, I assess Guthrie’s own childness, expressed through his behaviour, language, and prolific creative outpourings, a quality enhanced by very specific biographical circumstances.

Practice effects, defined as improvements in cognitive test performance due to repeated exposure to the test materials, have traditionally been viewed as sources of error. However, they might provide useful information for predicting cognitive outcome. The current study used three separate patient samples (older adults with mild cognitive impairments, individuals who were HIV +, individuals with Huntington's disease) to examine the relationship between practice effects and cognitive functioning at a later point. Across all three samples, practice effects accounted for as much as 31 to 83% of the variance in the follow-up cognitive scores, after controlling for baseline cognitive functioning. If these findings can be replicated in other patients with neurodegenerative disorders, clinicians and researchers may be able to develop predictive models to identify the individuals who are most likely to demonstrate continued cognitive decline across time. The ability to utilize practice effects data would add a simple, convenient, and non-invasive marker for monitoring an individual patient's cognitive status. Additionally, this prognostic index could be used to offer interventions to patients who are in the earliest stages of progressive neurodegenerative disorders. Practice effects, defined as improvements in cognitive test performance due to repeated evaluation with the same test materials, have traditionally been viewed as sources of error variance rather than diagnostically useful information. Recently, however, it has been suggested that this psychometric phenomenon might prove useful in predicting cognitive outcome. For example, Darby et al. (2002) repeatedly administered a computerized battery of cognitive tasks to a group of patients with Mild Cognitive Impairment (MCI) and matched controls over the course of a single day. The results of this study indicated that healthy control

RESUMO Este texto tem por meta analisar um conjunto documental pouco explorado referente às pesquisas do médico Raimundo Nina Rodrigues sobre fenômenos coletivos registrados entre o final do século XIX e inicio do XX. Pretendemos dar ênfase a algumas reflexões do referido autor e, especialmente, ao diálogo que ele estabeleceu com profissionais estrangeiros do campo da sociologia, da antropologia e da saúde mental. O esforço intelectual de Nina é como um testemunho do nascimento de um campo de estudos cujas primeiras linhas estavam sendo traçadas no Brasil: a psicologia das massas ou loucura das multidões. Nina resgata uma rica tradição de estudos para abordar, à sua maneira, casos de epidemias coletivas e religiosas no Brasil, vinculadas à população negra e mestiça. Palavras-chave Nina Rodrigues – multidões – loucura – religião – miscigenação. ABSTRACT This text is aimed to analyse an underexplored set of documents related to the research referring to the physician Raimundo Nina Rodrigues on collective phenomena recorded between the late nineteenth and early twentieth centuries. We intend to emphasize some reflections of that author and especially the dialogue which he established with foreign professionals in the field of sociology, anthropology and mental health.Ninàs intellectual effort is like a witness of the birth of a field of study whose first lines were being drawn in Brazil: crowd psychology or the madness of crowds. Nina rescues a rich tradition of studies to address, in its way, cases of collective and religious epidemics in Brazil, linked to the black and miscegenated population. Keywords Nina Rodrigues – crowds – madness – religion – miscegenation. Introdução É possível afirmar que Raimundo Nina Rodrigues foi um dos primeiros intelectuais brasileiros a, sistematicamente, teorizar e formular hipóteses sobre o campo da chamada Psicologia das Multidões. Esse aspecto foi apontado, pela primeira vez pelo médico Arthur de Araújo Pereira Ramos (1903-1949) no prefácio do livro As collectividades anormais, coletânea de textos de Nina Rodrigues, reunida pelo primeiro em 1939: Nina Rodrigues, já apontado como o iniciador dos estudos de etnografia e psicologia social do negro, no Brasil, já conhecido como estudioso de nossos problemas de raça e de cultura, aclamado como uma das autoridades em criminologia e ciência penal.... talvez não fosse lembrado, pela nossa pobre ciência nacional, tão esquecida dos precursores, como um dos pioneiros do movimento da psicologia coletiva. No entanto o seu nome fora apontado pelos estudiosos europeus, como um dos fundadores da psicologia das multidões, um dos criadores da psicologia gregária, normal e patológica, ao lado dos Rossi, dos Si

this study was
constructed to establish the endogenous and overexpressed, wild type and mutant, full
length (FL) and truncated htt localizations in cell lines and in HD mouse models. These
various constructs, run under the same experimental conditions are expected to provide a
full delineation of htt localization. In this regard, the expression pattern of endogenous and
overexpressed htt was investigated in neuronal and non-neuronal cell lines (HEK 293, N2A,
PC12, IMR32) and embryonic striatal neurons of R6/1 and HdhQ150 mice expressing
truncated and FL htt, respectively. In addition to localization studies, 3D htt structure was
analyzed using fold recognition model and in silico polyQ expansion mutations were created in the htt protein using VMD programme which will help to decipher the effects of the mutation in  protein structure and function.

Polyglutamine (polyQ) diseases are incurable neurological disorders caused by CAG repeat expansion in the open reading frames (ORFs) of specific genes. This type of mutation in the HTT gene is responsible for Huntington's disease (HD). CAG repeat-targeting artificial miRNAs (art-miRNAs) were shown as attractive therapeutic approach for polyQ disorders as they caused allele-selective decrease in the level of mutant proteins. Here, using polyQ disease models, we aimed to demonstrate how miRNA-based gene expression regulation is dependent on target sequence features. We show that the silencing efficiency and selectivity of art-miRNAs is influenced by the localization of the CAG repeat tract within transcript and the specific sequence context. Furthermore, we aimed to reveal the events leading to downregulation of mutant polyQ proteins and found very rapid activation of translational repression and HTT transcript deadenylation. Slicer-activity of AGO2 was dispensable in this process, as determined in AGO2 knockout cells generated with CRISPR-Cas9 technology. We also showed highly allele-selective downregulation of huntingtin in human HD neural progenitors (NPs). Taken together, art-miRNA activity may serve as a model of the cooperative activity and targeting of ORF regions by endogenous miRNAs.

Movement disorders can be defined as neurological syndromes presenting with excessive or diminished automatic or voluntary movements not related to weakness or spasticity. Both Parkinson’s disease (PD) and Huntington’s disease (HD) are well-known examples of these syndromes. The high prevalence of comorbid psychiatric symptoms like depres- sion, anxiety, obsessive-compulsive symptoms, hallucinations, delusions, impulsivity, sleep disorders, apathy and cognitive impairment mean that these conditions must be regarded as neuropsychiatric diseases. In this article, we review neuroanatomical (structural and functional), psychopathological and neuropsychological aspects of PD and HD. The role of fronto-subcortical loops in non-motor functions is particularly emphasised in order to understand the clinical spectrum of both diseases, together with the influence of genetic, psychological and psychosocial aspects. A brief description of the main psychopharmacological approaches for both diseases is also included

Tardive dyskinesia (TD) is a movement disorder secondary to neuroleptic treatment. Whether TD is associated with neurocognitive dysfunction is a controversial issue. We reviewed 31 published studies evaluating neuropsychological (NP) test results in schizophrenic patients with and without TD and found that TD was generally reported to be associated with cognitive impairment. Numerous methodological limitations, however, restrict the conclusions made about the relationship between cognition and dyskinesia. We therefore undertook a study in which 143 schizophrenic patients were evaluated on a comprehensive NP test battery. On both global and learning deficit scores, TD patients demonstrated greater impairment than did a matched comparison group. Two aspects of TD (severity and topography) were related to severity of cognitive impairment. These findings suggest that dyskinesia and cognition may share some underlying mechanism in schizophrenia.

In this article, I reflect on my experiences as someone with Huntington's Disease who works professionally as a development ethnomusicologist, and who creates musical, video, and graphic arts for healing in communities I know. People struggling with disease and trauma benefit enormously by identifying their needs and goals, finding and valuing their artistic resources, and sparking creativity from within their and their social networks' artistry that addresses those needs. Therapists and others can contribute to these processes best by using methods that include eliciting artistic biographies, sparking community creativity, and becoming multiartistic activists.

Testing Knowledge: Toward an Ecology of Diagnosis (Dingdingdong, 2015) pursues the question of taming the violence of the new species of medical foreknowledge represented by genetic testing. Adopting historical and epistemological perspectives on diagnostic situations, including observations from anthropological field research, speculative storytelling, and ancient oracles, Testing Knowledge proposes a new ecology of predictive diagnostic gestures, which potentially concern us all.

La enfermedad de Huntington es una enfermedad de etiología genética con herencia autosómica dominante en la que la repetición anormal de la tripleta CAG produce de una
proteína anormal (huntingtina). Se caracteriza por manifestaciones clínicas como corea, ataxia y demencia.
Presenta morbilidad asociada con múltiples alteraciones psiquiátricas, la más frecuente de las cuales es la depresión, que se presenta en la mitad de los pacientes, aproximadamente. Se presentan, también, psicosis, irritabilidad, apatía, síntomas obsesivos y delirium. No existe cura para la enfermedad y las intervenciones se dirigen al tratamiento sintomático de las alteraciones del movimiento y de la sintomatología psiquiátrica.

Abstract

Huntington disease is an autosomal dominantly transmitted disorder. Huntingtin is the abnormal protein produced by the repeat ofthe CAG triplet. It is characterized by motor
abnormalities, cognitive dysfunction and dementia.
It has comorbidity with psychiatric manifestations like depression, present in half of the patients. Psychosis, irritability, apathy, obsessive symptoms and delirium may be present too. There is no cure for the disease. Interventions are aimed to treat symptoms like motor abnormalities and psychiatric manifestations."

Article abstract-We administered the Mattis Dementia Rating Scale (DRS) to 120 patients to evaluate the effect of dementia severity on distinct cognitive profiles. Sixty patients with Huntington's disease (HD) and 60 patients with Alzheimer's disease (AD) were separated by dementia severity into three groups: mildly demented (DRS mean total = 1291, moderately demented (DRS mean total = 117), and severely demented (DRS mean total = 102). At all levels of de-mentia severity, HD patients demonstrated greater impairment than AD patients on the Initiatioflerseveration sub-scale, whereas AD patients demonstrated greater impairment than HD patients on the Memory subscale. At moderate and severe levels of dementia, HD patients demonstrated a n additional impairment in constructional praxis. These profile differences were independent of dementia severity and continued to differentiate between so-called cortical and subcortical dernentias in later stages of dementia severity. NEUROLOGY 1995;45:951-956

Abstract: A sense of balance, smooth controlled movements, such as walking are guided by the basal ganglia. The ability to recognize disgust in another person's face is also associated with the basal ganglia. People with a diagnosis of Huntington's disease lose both the ability to walk and move in a smooth controlled way and the ability to recognize disgust. Exercise and movement has been shown to light up the basal ganglia and slow the deterioration. Imagining something disgust also lights up the basal ganglia. Thesis based on client results: Spending a few minutes a day thinking about a disgusting food can light up, bring better blood flow and function to the basal ganglia, resulting in better movement and brain health.

Keywords: disgust, basal ganglia, disgust exercises, Huntington's disease, ataxia, walking, brain health

Burnham, Kimberly Burnham (2013). "Disgust Exercises for Balance: A Third Culture Kids Perspective on the World, Food and the Brain: Disgusting Foods, Beautiful Truth Poster Presentation." Poster Presentation accepted at the Neuroplasticity and Cognitive Modifiability Conference Jerusalem, Israel June 2013.: [Full Text]  https://www.academia.edu/17427646/Disgust_Exercises_for_Balance_A_Third_Culture_Kids_Perspective_on_the_World_Food_and_the_Brain_Disgusting_Foods_Beautiful_Truth_Poster_Presentation

Over the recent years, Huntington's disease (HD) has become widely discussed in the scientific literature especially because at the mutant level there are several contradictions regarding the aggregation mechanism. The specific role of the physiological huntingtin protein remains unknown, due to the lack of characterization of its entire crystallographic structure, making the experimental and theoretical research even harder when taking into consideration its involvement in multiple biological functions and its high affinity for different interacting partners. Different types of models, containing fewer (not more than 35 Qs) polyglutamine residues for the WT structure and above 35 Qs for the mutants, were subjected to classical or advanced MD simulations to establish the proteins' structural stability by evaluating their conformational changes. Outside the polyQ tract, there are two other regions of interest (the N17 domain and the polyP rich domain) considered to be essential for the aggregation kinetics at the mutant level. The polymerization process is considered to be dependent on the polyQ length. As the polyQ tract's dimension increases, the structures present more β-sheet conformations. Contrarily, it is also considered that the aggregation stability is not necessarily dependent on the number of Qs, while the initial stage of the aggregation seed might play the decisive role. A general assumption regarding the polyP domain is that it might preserve the polyQ structures soluble by acting as an antagonist for β-sheet formation.

Background: Huntington's Disease is an irreversible neurodegenerative disease characterized by the progressive deterioration of specific brain nerve cells. The current evaluation of cellular and physiological events in patients with HD relies on the development of transgenic animal models. To explore such events in vivo, diffusion tensor imaging has been developed to examine the early macro and microstructural changes in brain tissue. However, the gap in diffusion tensor imaging findings between animal models and clinical studies and the lack of microstructural confirmation by histological methods has questioned the validity of this method. Objective: This review explores white and grey matter ultrastructural changes associated to diffusion tensor imaging, as well as similarities and differences between preclinical and clinical Hun-tington's Disease studies. Methods: A comprehensive review of the literature using online-resources was performed (Pub-Med search). Results: Similar changes in fractional anisotropy as well as axial, radial and mean diffusivities were observed in white matter tracts across clinical and animal studies. However, comparative diffusion alterations in different grey matter structures were inconsistent between clinical and animal studies. Conclusion: Diffusion tensor imaging can be related to specific structural anomalies in specific cellular populations. However, some differences between animal and clinical studies could derive from the contrasting neuroanatomy or connectivity across species. Such differences should be considered before generalizing preclinical results into the clinical practice. Moreover, current limitations of this technique to accurately represent complex multicellular events at the single micro scale are real. Future work applying complex diffusion models should be considered.

The CAG repeat expansion in the Huntington’s disease gene HTT extends a polyglutamine tract in mutant huntingtin that enhances its ability to facilitate polycomb repressive complex 2 (PRC2). To gain insight into this dominant gain of function, we mapped histone modifications genome-wide across an isogenic panel of mouse embryonic stem cell (ESC) and neuronal progenitor cell (NPC) lines, comparing the effects of Htt null and different size Htt CAG mutations. We found that Htt is required in ESC for the proper deposition of histone H3K27me3 at a subset of ‘bivalent’ loci but in NPC it is needed at ‘bivalent’ loci for both the proper maintenance and the appropriate removal of this mark. In contrast, Htt CAG size, though changing histone H3K27me3, is prominently associated with altered histone H3K4me3 at ‘active’ loci. The sets of ESC and NPC genes with altered histone marks delineated by the lack of huntingtin or the presence of mutant huntingtin, though distinct, are enriched in similar pathways with apoptosis specifically highlighted for the CAG mutation. Thus, the manner by which huntingtin function facilitates PRC2 may afford mutant huntingtin with multiple opportunities to impinge upon the broader machinery that orchestrates developmentally appropriate chromatin status.


The implementation of cell replacement therapies for Huntington’s disease using multipotent neural stem cells (NSCs) requires the specific differentiation into g-aminobutyric acid (GABA) neuronal subtype before transplantation. Here we present an efficient culture procedure that induces stable GABAergic neurons from the immortalized striatal neural stem cell line ST14A. This process requires sequential retinoic acid treatment and KCl depolarization. Initial addition of 10 AM retinoic acid increased cell survival and promoted neuronal differentiation. Subsequent stimulation with 40 mM KCl induced specific differentiation into GABAergic neurons, yielding 74% of total cultured cells. KCl-evoked Ca2+ influx reduced cell proliferation and nestin expression, and induced neurite outgrowth and GABAergic markers as well as GABA contents, release, and uptake. Characterization of the integration, survival, and phenotype of these predifferentiated GABAergic neurons following transplantation into the adult brain in a model of Huntington’s disease revealed long-term survival in quinolinate-lesioned striata. Under these conditions, cells maintained their GABAergic phenotype and elaborated neurite processes with synaptic contacts with endogenous neurons. In conclusion, we have generated a homogeneous population of functional GABAergic neurons from a neural stem cell line, which survive and maintain their acquired fate in vivo. These data may lend support to the possibility of cell replacement therapies for Huntington’s disease using neural stem cells.

This paper describes enhancements to automate classification of brain tissues for multi-site degenerative magnetic resonance imaging (MRI) data analysis. Processing of large collections of MR images is a key research technique to advance our understanding of the human brain. Previous studies have developed a robust multi-modal tool for automated tissue classification of large-scale data based on expectation maximization (EM) method initialized by group-wise prior probability distributions. This work aims to augment the EM-based classification using a non-parametric fuzzy k-Nearest Neighbor (k-NN) classifier that can model the unique anatomical states of each subject in the study of degenerative diseases. The presented method is applicable to multi-center heterogeneous data analysis and is quantitatively validated on a set of 18 synthetic multi-modal MR datasets having six different levels of noise and three degrees of bias-field provided with known ground truth. Dice index and average Hausdorff distance are used to compare the accuracy and robustness of the proposed method to a state-of-the-art classification method implemented based on EM algorithm. Both evaluation measurements show that presented enhancements produce superior results as compared to the EM only classification.

Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder caused by an unstable expansion of CAG repeats in the HD gene. The symptoms include cognitive dysfunction and severe motor impairments. The neuropathology is characterized by neuronal loss mainly in the striatum and cortex, although other regions including the hippocampus are also affected. In this review we discuss the different mouse models of HD, and how the process of neurogenesis in the dentate gyrus (DG) of the hippocampus and the subventricular zone (SVZ) is affected in each. Deficits in adult hippocampal neurogenesis have been repeatedly shown in different genetic models of HD, raising the possibility that an impairment of the neurogenic process might underlie some of the cognitive deficits associated with this neurodegenerative disorder. On the other hand, an increase in SVZ neurogenesis has been observed in human HD brains while no differences in SVZ cell proliferation have been detected in the mouse models. In this review we will discuss the discrepancies between these findings as well as the several mechanisms that might contribute to a dysregulation of adult neurogenesis in HD. Finally, we will provide an overview of the various therapeutic strategies aimed at stimulating the endogenous neurogenic capacity that have been tested in HD genetic models. Ultimately, the insights obtained from these and future studies will greatly improve our understanding of the cognitive impairment characteristic of HD.

Excessive and sustained exposure to glutamate leads to injurious elevations of cytosolic calcium ([Ca2 +]i), generation of reactive oxygen and nitrogen species (ROS, RNS), mitochondrial failure, mobilization of intracellular zinc ([Zn2 +]i), and, ultimately, neuronal death. The relative contribution and temporal dynamics of the activation of these processes to promote the full development of excitotoxicity are still not completely understood. In this study, we exploited the unique features of nNOS positive neurons [nNOS (+)], a striatal subpopulation that is constitutively spared from NMDAR-dependent insults, and dissected NMDAR-driven [Ca2 +]i, [Zn2 +]i, ROS, and mitochondrial changes occurring in these neurons and the overall population of nNOS (-) striatal neurons. Comparing the two populations and employing pharmacological, biochemical, and single-cell imaging techniques, we show that [Zn2 +]i mobilization acts as critical intermediate in the cascade that links NMDAR-mediated ROS overproduction, mitochondrial failure, and [Ca2 +]i deregulation to the production of neuronal damage. Results of this study may also provide the rationale for aiming at therapeutic agents that favor Zn2 + homeostasis for the treatment of acute or chronic neurological conditions associated with excitotoxicity.

Huntington's disease (HD) is a movement disorder characterized by the early selective degeneration of the basal ganglia and the striatum in the brain. It shows decreases in the inputs from the sensory motor system. One way to increase input reaching the basal ganglia is to increase sensory and motor stimulus. This can be particularly effective when the input targets specific areas of dysfunction, such as the globus pallidus

International Journal of Complementary & Alternative Medicine  ISSN: 2381-1803IJCAM http://medcraveonline.com/IJCAM/ http://medcraveonline.com/associateEditorRegistration.php

Citation: Burnham K (2016) Disgusting Foods, Pure Water and Beautiful Truth for Balanced Muscle Control. Int J Complement Alt Med 3(1): 00055.
DOI: 10.15406/ijcam.2016.03.00055 http://medcraveonline.com/IJCAM/IJCAM-03-00055.pdf

Abstract: The author proposes that conscious awareness of disgust or disgust exercises can decrease tremors, and muscle rigidity, as well as support other functions of the basal ganglia, insula, hypothalamus, and the cerebellum. Pattern recognition skills needed to experience and identify disgust in the faces of others is compromised in people with brain dysfunctions like depression, bipolar disorder, associated with sensory dysfunctions and mood, Huntington’s disease (a genetic movement disorder), focal dystonia (unusually tight twisted muscles), Parkinson’s disease (tremor and movement disorder), Wilson’s disease (genetic copper processing disorder), and Velo-cardio-facial syndrome (a genetic disorder associated with interstitial deletions of chromosome 22q11.2). Disgust exercises or consciously paying attention to what is disgusting and what is pleasant or beautiful may trigger changes in the basal ganglia, where disgust is perceived and lead to improvements in balance, walking, tremors, obsessive compulsive disorder symptoms, depression, and overall brain function. The different functions of a particular brain structure can be considered doorways into healing. The basal ganglia and the neurochemical dopamine have responsibilities for disgust recognition, suppressing tremors as well as other unwanted muscle movements by balancing motor input from other areas of the brain, and preventing muscle rigidity.

Keywords: Disgust; Brain health; Basal ganglia; Dopamine; Parkinson’s; Tremors;
Huntington’s ataxia; Balance

Kimberly Burnham, PhD joins the International Journal of Complementary & Alternative Medicine  ISSN: 2381-1803IJCAM http://medcraveonline.com/IJCAM/editorial-board as an associate editor along with:
Honorable Editors: W John Martin, Institute of Progressive Medicine, USA; Daniel Weber, National Cancer Institute, Australia; Edward Frederick Block, Block Institute for Astrobiological Studies, USA; Janusz Wrobel, Oakland University, USA; Harvey Milkman, Metropolitan State College of Denver, USA; Acharya Girish Jha, Shreyas USA LLC, USA; Cornelis Peters, Europa Ayurveda Centrum, Netherlands; William A Courson, Bodhananda Vedic Institute School of Ayurveda, USA; Michael J Gonzalez, The University of Puerto Rico Medical Sciences, USA; Jeffrey Ruterbusch, Central Michigan University, USA; Eugene R Zampieron, University of Bridgeport College of Naturopathic Medicine, USA; Virender Sodhi, Ayurvedic and Naturopathic medical Clinic, USA; Joseph J Collins, Your Hormones Inc., USA; Habil Hegyi Gabriella, Pecs University, Hungary area; Andrew W Campbell, Clinica del Barrio LLC, USA; Anthony B James, Oklevueha Native American Church of SomaVeda, USA; Ian Hamilton, Art and Homeopathy Group, United Kingdom; Robert C Angus, Celebration Of Health, USA; Bernardo Merizalde,
Thomas Jefferson University, USA; Robelyn Garcia, Arizona State University and Senior University, USA; Gary J Neuger, Intelligent Hypnotherapy LLC, USA; Robert O Young, Universal Medical Imaging Group, USA; Aileen Chan
Chinese University of Hong Kong, China; J G Moellendorf, Moellendorf Chiropractic Office, Ltd., USA; Debbie Novick, Novick Integrated Medicine, USA; Jim Copeland, Copeland Chiropractic & Acupuncture, USA; Steven Gurgevich, The University of Arizona College of Medicine, USA; Sudha Carolyn Lundeen, Kripalu Center for Yoga and Health, USA; Harvey Kaltsas, Healing Centre Limited Liability Company, USA; Graeme Tobyn, University of Central Lancashire, United Kingdom;

Associate Editors: Vernon A Barnes, Georgia Regents University, USA; Harry Rotteveel, FemHealth, Netherlands; Helena Zhang, Emperors College, USA; Thierry Clerc, Metabolic Balance Cambridge, United Kingdom; Dong-Yuan Cao, Xian Jiaotong University Health Science Center, China; Sean H Thompson, Concorde Career College, USA; Sonya Patel, Mirvana Acupuncture and Chinese Herbs, USA; Debbie Papadakis, Hypno Healing Institute Inc., Canada; Boaz Bo ItsHaky, University of Bridgeport, USA; Kimberly Burnham, Akamai University & The Creating Calm Publishing Group, USA; and Rini Shamal, The Sanctuary Wellness Center & Yoga Studio, USA.

International Journal of Complementary and Alternative Medicine is an interdisciplinary peer-reviewed Open Access journal, considers articles on interventions and resources that complement or replace conventional therapies.
This journal aims to publish hypothesis-driven and evidence-based articles and is committed to publishing scholarly research articles, review articles, mini-review, short communications, case studies, editorial commentary and opinions, book reviews in area the of the Complementary and Alternative Medicine as a whole and encourages rigorous research.
Email: cam@medcraveonline.org, cam@medcraveonline.us

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Kimberly Burnham, PhD

A brain health expert, Kimberly Burnham has a PhD in Integrative Medicine (2006) from Westbrook University. She specializes in using complementary and alternative medicine to decrease symptoms in people with chronic pain, Parkinson's disease, Alzheimer's, Multiple Sclerosis, Huntington's ataxia, autism and other brain related issues.

She is the author of a number of books including: Parkinson's Alternatives; Regain Your Balance: Ataxia Solutions; and Our Fractal Nature, a Journey of Self-Discovery and Connection.  A clinician with a diverse background, Kimberly is also an award winning poet and published in the Inner Child Press poetry anthologies: Healing Through Words and World Healing, World Peace. 

A social media expert, Kimberly blogs regularly with a column on the intersection between healing traditions and faith on the Interfaith News Site, SpokaneFavs as well as writing a column entitled Community of Humanity in the Inner Child Magazine. She is faculty at Akamai University and the Master Mind University and has presented at the Raising Consciousness Now Summit, Spokane Chronic Pain Conference, Defeat Autism Now (DAN) Conference, Connecticut Arthritis Association Annual Meetings and other international conferences.

She sees individuals at New Moon Family Wellness in Spokane, Washington and does health coaching and consulting via phone or skpye with clients worldwide. Occasionally she will work in clinics around the world for a week or so consulting with local therapists and specializing in helping people with brain, spine, and nervous system issues. She can be reached through her website www.KimberlyBurnhamPhD.com or email NerveWhisperer@gmail.com