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1.
Dement. neuropsychol ; 15(1): 41-50, Jan.-Mar. 2021. tab, graf
Article in English | LILACS | ID: biblio-1286171

ABSTRACT

ABSTRACT. Clinical trials of the effects of physical activity have reported improvements in symptoms and quality of life in patients with Parkinson's disease (PD). Additionally, morphological brain changes after exercising were reported in PD animal models. However, these lifestyle-related changes were not evaluated in postmortem brain tissue. Objective: We aimed to evaluate, by immunohistochemistry, astrocytes, tyrosine hydroxylase (TH) and structural proteins expression (neurofilaments and microtubules — MAP2) changes in postmortem brain samples of individuals with Lewy body pathology. Methods: Braak PD stage≥III samples, classified by neuropathology analysis, from The Biobank for Aging Studies were classified into active (n=12) and non-active (n=12) groups, according to physical activity lifestyle, and paired by age, sex and Braak staging. Substantia nigra and basal ganglia were evaluated. Results: Groups were not different in terms of age or gender and had similar PD neuropathological burden (p=1.00). We observed higher TH expression in the active group in the substantia nigra and the basal ganglia (p=0.04). Astrocytes was greater in the non-active subjects in the midbrain (p=0.03) and basal ganglia (p=0.0004). MAP2 levels were higher for non-active participants in the basal ganglia (p=0.003) and similar between groups in the substantia nigra (p=0.46). Neurofilament levels for non-active participants were higher in the substantia nigra (p=0.006) but not in the basal ganglia (p=0.24). Conclusion: Active lifestyle seems to promote positive effects on brain by maintaining dopamine synthesis and structural protein expression in the nigrostriatal system and decrease astrogliosis in subjects with the same PD neuropathology burden.


RESUMO. Estudos dos efeitos da atividade física relataram melhora nos sintomas e na qualidade de vida de pacientes com doença de Parkinson (DP). Além disso, alterações morfológicas do cérebro após o exercício físico foram relatadas em modelos animais da DP. No entanto, essas mudanças relacionadas ao estilo de vida não foram avaliadas em tecido cerebral post-mortem. Objetivo: Avaliar a expressão de astrócitos, tirosina hidroxilase (TH) e a expressão de proteínas estruturais (neurofilamentos e microtúbulos — MAP2) por imuno-histoquímica, em amostras cerebrais post-mortem de indivíduos com corpos de Lewy. Métodos: Amostras com estágio de Braak para DP≥III, classificação neuropatológica, fornecidas pelo biobanco de estudos do envelhecimento foram classificadas em grupos ativos (n=12) e não ativos (n=12), de acordo com o estilo de vida (atividade física), e pareados por idade, sexo e estadiamento de Braak. Analisou-se a substância negra e gânglios da base. Resultados: Idade, sexo e classificação para DP foram semelhantes (p=1,00). Observou-se maior expressão de TH no grupo ativo (p=0,04). Amostras de não ativos revelaram maior expressão de astrócitos no mesencéfalo (p=0,03) e nos gânglios da base (p=0,0004); MAP2 nos gânglios da base (p=0,003); os níveis de neurofilamentos foram maiores na substância negra (p=0,006). Conclusão: O estilo de vida ativo parece promover efeitos positivos no cérebro, mantendo a síntese de dopamina e a expressão estrutural de proteínas no sistema nigrostriatal e com diminuição da ativação de astrócitos em indivíduos com a mesma classificação neuropatológica para a DP.


Subject(s)
Humans , Parkinson Disease , Lewy Bodies , Autopsy , Aging , Dopamine , Astrocytes , Life Style
2.
Article in English | WPRIM | ID: wpr-765866

ABSTRACT

The aggregation of α-synuclein (α-syn) has been implicated in the pathogenesis of many neurodegenerative disorders, including Parkinson's disease (PD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA). Postmortem analyses of α-syn pathology, especially that of PD, have suggested that aggregates progressively spread from a few discrete locations to wider brain regions. The neuron-to-neuron propagation of α-syn has been suggested to be the underlying mechanism by which aggregates spread throughout the brain. Many cellular and animal models has been created to study cell-to-cell propagation. Recently, it has been shown that a single injection of preformed fibrils (PFFs) made of recombinant α-syn proteins into various tissues and organs of many different animal species results in widespread α-syn pathology in the central nervous system (CNS). These PFF models have been extensively used to study the mechanism by which aggregates spread throughout the brain. Here, we review what we have learned from PFF models, describe the nature of PFFs and the neuropathological features, neurophysiological characteristics, and behavioral outcomes of the models.


Subject(s)
alpha-Synuclein , Animals , Brain , Central Nervous System , Dementia , Lewy Bodies , Models, Animal , Multiple System Atrophy , Neurodegenerative Diseases , Parkinson Disease , Pathology
3.
Article in English | WPRIM | ID: wpr-765840

ABSTRACT

OBJECTIVE: To clarify the specificity of the ‘hot cross bun’ sign (HCBS) for multiple system atrophy (MSA) in adult cerebellar ataxia or parkinsonism. METHODS: The radiologic information systems at an academic center and affiliated veterans' hospital were queried using the keywords ‘hot cross bun,’ ‘pontocerebellar,’ ‘cruciate,’ ‘cruciform,’ ‘MSA,’ ‘multiple system atrophy,’ and ‘multisystem atrophy.’ Scans were reviewed by a neurologist and neuroradiologist to identify the HCBS. Subjects with the HCBS were reviewed by 2 neurologists to identify the most likely etiology of the patient's neurologic symptoms. RESULTS: Eleven cases were identified. Etiologies included MSA (4 probable, 2 possible), hereditary cerebellar ataxia (3/11), probable dementia with Lewy bodies (1/11), and uncertain despite autopsy (1/11). CONCLUSION: MSA was the most common etiology. However, 5 of the 11 patients did not have MSA. The most common alternate etiology was an undefined hereditary cerebellar ataxia (3/11).


Subject(s)
Adult , Autopsy , Cerebellar Ataxia , Dementia , Hexachlorobenzene , Humans , Lewy Bodies , Magnetic Resonance Imaging , Multiple System Atrophy , Neurologic Manifestations , Olivopontocerebellar Atrophies , Parkinsonian Disorders , Radiology Information Systems , Sensitivity and Specificity
4.
Experimental Neurobiology ; : 547-553, 2019.
Article in English | WPRIM | ID: wpr-763791

ABSTRACT

Synucleinopathies are neurodegenerative disorders characterized by the progressive accumulation of α-synuclein (α-syn) in neurons and glia and include Parkinson's disease (PD) and dementia with Lewy bodies (DLB). In this review, we consolidate our key findings and recent studies concerning the role of Toll-like receptor 2 (TLR2), a pattern recognition innate immune receptor, in the pathogenesis of synucleinopathies. First, we address the pathological interaction of α-syn with microglial TLR2 and its neurotoxic inflammatory effects. Then, we show that neuronal TLR2 activation not only induces abnormal α-syn accumulation by impairing autophagy, but also modulates α-syn transmission. Finally, we demonstrate that administration of a TLR2 functional inhibitor improves the neuropathology and behavioral deficits of a synucleinopathy mouse model. Altogether, we present TLR2 modulation as a promising immunotherapy for synucleinopathies.


Subject(s)
Animals , Autophagy , Dementia , Immunotherapy , Lewy Bodies , Mice , Neurodegenerative Diseases , Neuroglia , Neurons , Neuropathology , Parkinson Disease , Toll-Like Receptor 2 , Toll-Like Receptors
5.
Experimental Neurobiology ; : 504-515, 2019.
Article in English | WPRIM | ID: wpr-763777

ABSTRACT

Parkinson’s disease (PD) is one of the late-onset neurodegenerative movement disorder. Major pathological markers of PD include progressive loss of dopaminergic neurons, Lewy body formation, genetic mutations, and environmental factors. Epigenetic regulation of specific gene expression via impaired histone acetylation is associated with neuronal dysfunction in various neurodegenerative diseases. In this study, we hypothesized that histone deacetylase (HDAC) inhibitor, valproic acid (VPA), can improve motor function by enhancing cell survival in PD genetic model mice with LRRK2 R1441G mutation. To address this question, we administered VPA in LRRK2 R1441G transgenic mice to determine whether VPA affects 1) histone acetylation and HDAC expression, 2) dopaminergic neuron survival, 3) inflammatory responses, 4) motor or non-motor symptoms. As results, VPA administration increased histone acetylation level and the number of tyrosine hydroxylase (TH) positive neurons in substantia nigra of LRRK2 R1441G mice. VPA reduced iba-1 positive activated microglia and the mRNA levels of pro-inflammatory marker genes in LRRK2 R1441G mice. In addition, VPA induced the improvement of PD-like motor and non-motor behavior in LRRK2 R1441G mice. These data suggest that the inhibition of HDAC can be further studied as potential future therapeutics for PD.


Subject(s)
Acetylation , Animals , Cell Survival , Dopaminergic Neurons , Epigenomics , Gene Expression , Histone Deacetylases , Histones , Lewy Bodies , Mice , Mice, Transgenic , Microglia , Models, Genetic , Movement Disorders , Neurodegenerative Diseases , Neurons , Neuroprotection , RNA, Messenger , Substantia Nigra , Tyrosine 3-Monooxygenase , Valproic Acid
6.
Article in Korean | WPRIM | ID: wpr-787397

ABSTRACT

Dementia with Lewy bodies(DLB) is the second most common neurodegenerative disease. However, DLB might not be adequately diagnosed due to its variety of clinical symptoms. The authors present 65-year-old Mrs. A. who showed Parkinson's movement, cognitive decline, psychological symptoms, and autonomic dysfunction. According to the clinical features and biological markers in the recently revised DLB criteria, Mrs. A. was diagnosed with probable DLB. Differential diagnoses of delirium, Parkinson's dementia, and Alzheimer's dementia were discussed. Psychopharmacological treatments of antidepressants or anxiolytics caused intolerable side effects and showed little efficacy to Mrs. A. She experienced two episodes of hyponatremia during her one-year treatment. Recovery from neurological symptoms due to the first hyponatremia was time-consuming, and in the second, it was associated with changes in the level of consciousness despite relatively mild hyponatremia. A fall that occurred in the latter part of treatment triggered remarkable deterioration of DLB symptoms and daily life function. Prevention of falls is important for maintaining the quality of life of patients with DLB.


Subject(s)
Accidental Falls , Aged , alpha-Synuclein , Anti-Anxiety Agents , Antidepressive Agents , Biomarkers , Consciousness , Delirium , Dementia , Diagnosis , Diagnosis, Differential , Humans , Hyponatremia , Lewy Bodies , Neurodegenerative Diseases , Quality of Life
7.
Article in English | WPRIM | ID: wpr-763298

ABSTRACT

OBJECTIVES: Parkinson disease (PD) is frequently associated with olfactory disorder at early stage, which is caused by deposition of Lewy bodies emerging from the olfactory bulb to higher olfactory centers. Early detection of olfactory disorder in the patients with PD may lead to the early diagnosis and treatment for this refractory disease. METHODS: Visual analog scale (VAS), Jet Stream Olfactometry, and Japanese smell identification test, Open Essence (OE), were carried out on 39 patients with PD. Thirty-one patients with postviral olfactory disorder (PVOD), which was caused by the olfactory mucosal dysfunction, were also enrolled in this study as control. RESULTS: There were no significant differences in detection thresholds (2.2 vs. 1.4, P=0.13), recognition thresholds (3.9 vs. 3.5, P=0.39) and OE (4.8 vs. 4.2, P=0.47) between PVOD and PD, while VAS scores of PVOD and PD were significantly different (2.0 and 6.2, P<0.01). In OE, significant differences were observed in the accuracy rates of menthol (68% vs. 44%, P=0.04) and Indian ink (42% vs. 15%, P=0.01) between PVOD and PD. Of particular interest, patients with PVOD tended to select “no detectable,” while patients with PD tended to select wrong alternative other than “no smell detected.” CONCLUSION: Discrepancy between VAS and OE, and high selected rates of wrong alternative other than “undetectable” in OE might be significant signs of olfactory dysfunction associated with PD.


Subject(s)
Asian Continental Ancestry Group , Early Diagnosis , Humans , Ink , Lewy Bodies , Menthol , Olfactometry , Olfactory Bulb , Parkinson Disease , Rivers , Smell , Visual Analog Scale
8.
Article in English | WPRIM | ID: wpr-765815

ABSTRACT

In recent years, several radiotracers that selectively bind to pathological tau proteins have been developed. Evidence is emerging that binding patterns of in vivo tau positron emission tomography (PET) studies in Alzheimer's disease (AD) patients closely resemble the distribution patterns of known neurofibrillary tangle pathology, with the extent of tracer binding reflecting the clinical and pathological progression of AD. In Lewy body diseases (LBD), tau PET imaging has clearly revealed cortical tau burden with a distribution pattern distinct from AD and increased cortical binding within the LBD spectrum. In progressive supranuclear palsy, the globus pallidus and midbrain have shown increased binding most prominently. Tau PET patterns in patients with corticobasal syndrome are characterized by asymmetrical uptake in the motor cortex and underlying white matter, as well as in the basal ganglia. Even in the patients with multiple system atrophy, which is basically a synucleinopathy, ¹⁸F-flortaucipir, a widely used tau PET tracer, also binds to the atrophic posterior putamen, possibly due to off-target binding. These distinct patterns of tau-selective radiotracer binding in the various degenerative parkinsonisms suggest its utility as a potential imaging biomarker for the differential diagnosis of parkinsonisms.


Subject(s)
Alzheimer Disease , Basal Ganglia , Diagnosis, Differential , Electrons , Globus Pallidus , Humans , Lewy Bodies , Mesencephalon , Motor Cortex , Multiple System Atrophy , Neurofibrillary Tangles , Parkinsonian Disorders , Pathology , Positron-Emission Tomography , Putamen , Supranuclear Palsy, Progressive , tau Proteins , White Matter
9.
Arq. neuropsiquiatr ; 75(10): 751-753, Oct. 2017.
Article in English | LILACS | ID: biblio-888257

ABSTRACT

ABSTRACT Fritz Heinrich Jakob Lewy described, for the first time, in 1912, novel peculiar inclusions in neurons of certain brain nuclei in patients with Paralysis agitans, and compared his finding to the amyloid bodies described by Lafora one year before. Gonzalo Rodriguez Lafora studied one patient with Paralysis agitans, in 1913, and recognized, described, and depicted structures identical to those previously reported by Lewy. He was the first to acknowledge Lewy's finding, and also the first to name such inclusions after the discoverer - cuerpos intracelulares de Lewy (Lewy bodies). Konstantin Nikolaevich Trétiakoff named the inclusions he found in neurons of the substantia nigra of patients with Parkinson's disease as corps de Lewy (Lewy bodies), in 1919. Trétiakoff has unanimously received the credit for the eponym. However, Lafora's earlier description should make him deserving of the authorship of the eponym.


RESUMO Fritz Heinrich Jakob Lewy descreveu pela primeira vez, em 1912, inclusões singulares inéditas em neurônios de certos núcleos do cérebro em casos de Paralysis agitans e comparou seu achado aos corpos amilóides, como descrito por Lafora um ano antes. Gonzalo Rodriguez Lafora estudou um caso de Paralysis agitans, em 1913,e reconheceu, descreveu e representou estruturas idênticas às recentemente relatadas por Lewy. Foi o primeiro a reconhecer o achado de Lewy e também o primeiro a denominar tais inclusões segundo seu descobridor - cuerpos intracelulares de Lewy (corpos de Lewy). Konstantin Nikolaevich Tretiakoff designou as inclusões que encontrou em neurônios da substantia nigra em casos de doença de Parkinson de corps de Lewy (corpos de Lewy), em 1919. Ele recebeu o crédito pelo epônimo de modo unânime. Entretanto, a descrição anterior de Lafora deveria fazê-lo merecedor da autoria do epônimo.


Subject(s)
Humans , History, 19th Century , History, 20th Century , Lewy Bodies , Eponyms , Neurology/history , Spain , Russia , Germany
10.
Dement. neuropsychol ; 11(2): 198-201, Apr.-June 2017.
Article in English | LILACS | ID: biblio-890997

ABSTRACT

ABSTRACT Fritz Jacob Heinrich Lewy described the pathology of Paralysis agitans [Parkinson disease] and was the first to identify eosinophilic inclusion bodies in neurons of certain brain nuclei, later known as Lewy bodies, the pathological signature of the Lewy body diseases. In 1912, he published his seminal study, followed soon after by an update paper, and 10 years later, in 1923, by his voluminous book, where he exhaustively described the subject. The publication provided extensive information on the pathology of Paralysis agitans, and the entirely novel finding of eosinophilic inclusion bodies, which would become widely recognized and debated in the future. His discovery was acknowledged by important researchers who even named the structure after him. However, after his last publication on the issue, inexplicably, he never mentioned his histopathological discovery again. Despite several hypotheses, the reasons that led him to neglect (reject) the structure which he so preeminently described have remained elusive.


RESUMO Fritz Jacob Heinrich Lewy descreveu a patologia da Paralysis agitans [doença de Parkinson] e identificou pela primeira vez corpos de inclusão eosinófílos em neurônios de certos núcleos cerebrais, conhecidos mais tarde como corpos de Lewy, assinatura patológica das doenças dos corpos de Lewy. Ele divulgou em 1912 seu trabalho seminal, seguido logo por um artigo de atualização e 10 anos depois, em 1923, seu volumoso livro onde detalhou exaustivamente o assunto. Ali ele trouxe extensa informação sobre a patologia da Paralysis agitans e um achado inteiramente novo, os corpos de inclusão eosinófilos, que seriam valorizados e largamente debatidos no futuro. Seu achado foi reconhecido por importantes pesquisadores que até designaram essa estrutura com seu nome. Entretanto, após sua última publicação sobre o assunto, inexplicavelmente , ele nunca mais mencionou sua descoberta histopatológica. Apesar de diversas hipóteses, a razão que o levou negligenciar (rejeitar) a estrutura, que teve a primazia de descrever, permaneceu desconhecida.


Subject(s)
Humans , Parkinson Disease , Inclusion Bodies , Lewy Bodies , Eosinophils
11.
Article in English | WPRIM | ID: wpr-152983

ABSTRACT

OBJECTIVE: Donepezil is used to improve cognitive impairment of dementia with Lewy bodies (DLB). Visuo-spatial dysfunction is a well-known symptom of DLB. Non-verbal Raven’s Colored Progressive Matrices (RCPM) were used to assess both visual perception and reasoning ability in DLB subjects treated with donepezil. METHODS: Twenty-one DLB patients (mean age, 78.7±4.5 years) were enrolled. RCPM assessment was performed at the time of starting donepezil and within one year after starting donepezil. RESULTS: There were significant improvements of RCPM in the total scores between one year donepezil treatment (p=0.013), in both Set A score (p=0.002) and Set AB score (p=0.015), but trend in the Set B score (p=0.083). CONCLUSION: Donepezil is useful for improving visuo-spatial impairment in DLB, but not for problem-solving impairment.


Subject(s)
Cholinesterase Inhibitors , Cognition Disorders , Dementia , Humans , Lewy Bodies , Lewy Body Disease , Spatial Processing , Visual Perception
12.
Article in English | WPRIM | ID: wpr-38089

ABSTRACT

Parkinson's disease (PD), the second most common neurodegenerative disorder after Alzheimer's disease, is characterized by the loss of nigral dopaminergic neurons. PD leads to a series of clinical symptoms, including motor and non-motor disturbances. α-synuclein, the major component of Lewy bodies, is a hallmark lesion in PD. In this review, we concentrate on presenting the latest research on the structure, distribution, and function of α-synuclein, and its interactions with PD. We also summarize the clinic applications of α-synuclein, which suggest its use as a biomarker, and the latest progress in α-synuclein therapy.


Subject(s)
alpha-Synuclein , Alzheimer Disease , Dopaminergic Neurons , Lewy Bodies , Neurodegenerative Diseases , Parkinson Disease
13.
Chonnam Medical Journal ; : 145-150, 2016.
Article in English | WPRIM | ID: wpr-788354

ABSTRACT

¹²³I-meta-iodobenzylguanidine (MIBG) has become widely applied in Japan since its introduction to clinical cardiology and neurology practice in the 1990s. Neurological studies found decreased cardiac uptake of ¹²³I-MIBG in Lewy-body diseases including Parkinson's disease and dementia with Lewy bodies. Thus, cardiac MIBG uptake is now considered a biomarker of Lewy body diseases. Although scintigraphic images of ¹²³I-MIBG can be visually interpreted, an average count ratio of heart-to-mediastinum (H/M) has commonly served as a semi-quantitative marker of sympathetic activity. Since H/M ratios significantly vary according to acquisition and processing conditions, quality control should be appropriate, and quantitation should be standardized. The threshold H/M ratio for differentiating Lewy-body disease is 2.0-2.1, and was based on standardized H/M ratios to comparable values of medium-energy collimators. Parkinson's disease can be separated from various types of parkinsonian syndromes using cardiac ¹²³I-MIBG, whereas activity is decreased on images of Lewy-body diseases using both ¹²³I-ioflupane for the striatum and ¹²³I-MIBG. Despite being a simple index, the H/M ratio of ¹²³I-MIBG uptake is reproducible and can serve as an effective tool to support a diagnosis of Lewy-body diseases in neurological practice.


Subject(s)
3-Iodobenzylguanidine , Cardiology , Dementia , Diagnosis , Japan , Lewy Bodies , Lewy Body Disease , Neurology , Nuclear Medicine , Parkinson Disease , Parkinsonian Disorders , Quality Control
14.
Article in Korean | WPRIM | ID: wpr-725340

ABSTRACT

Dementia with Lewy bodies (DLB) is the second most common causes of dementia. It can exhibit a variety of clinical symptoms including cognitive decline, cognitive fluctuation, visual hallucinations, parkinsonism, REM sleep behavior disorder, hypersensitivity to neuroleptics and autonomic dysfunctions. Despite more well-known criteria for DLB, there are often misdiagnosis and inappropriate treatment. It gives a lot of clinical burden to the clinician as well as to patients and families. When reducing the misdiagnosis, the burden of all will be reduced. The special concern and solicitation are needed in order not to miss the diagnosis when the cardinal features of DLB may not be volunteered by patients and the caregivers. To control the symptoms, clinicians must find and reduce drugs that can have the negative effects on DLB symptoms. There is limited evidence about specific interventions but available data suggest cholinesterase inhibitors improve the cognitive and behavioral symptoms and menmantine slightly improves the global impression.


Subject(s)
Antipsychotic Agents , Behavioral Symptoms , Caregivers , Cholinesterase Inhibitors , Dementia , Diagnosis , Diagnostic Errors , Hallucinations , Humans , Hypersensitivity , Lewy Bodies , Parkinsonian Disorders , REM Sleep Behavior Disorder
15.
Experimental Neurobiology ; : 113-119, 2016.
Article in English | WPRIM | ID: wpr-213646

ABSTRACT

Synucleinopathies are a collection of neurological diseases that are characterized by deposition of α-synuclein aggregates in neurons and glia. These diseases include Parkinson's disease (PD), dementia with Lewy bodies, and multiple system atrophy. Although it has been increasingly clear that α-synuclein is implicated in the pathogenesis of PD and other synucleinopathies, the precise mechanism underlying the disease process remains to be unraveled. The past studies on how α-synuclein exerts pathogenic actions have focused on its direct, cell-autonomous neurotoxic effects. However, recent findings suggested that there might be indirect, non-cell-autonomous pathways, perhaps through the changes in glial cells, for the pathogenic actions of this protein. Here, we present evidence that α-synuclein can cause neurodegeneration through a non-cell-autonomous manner. We show that α-synuclein can be secreted from neurons and induces inflammatory responses in microglia, which in turn secreted neurotoxic agents into the media causing neurodegeneration. The neurotoxic response of microglia was mediated by activation of toll-like receptor 2 (TLR2), a receptor for neuron-derived α-synuclein. This work suggests that TLR2 is the key molecule that mediates non-cell-autonomous neurotoxic effects of α-synuclein, hence a candidate for the therapeutic target.


Subject(s)
Dementia , Lewy Bodies , Microglia , Multiple System Atrophy , Neuroglia , Neurons , Parkinson Disease , Toll-Like Receptor 2 , Toll-Like Receptors
16.
Chonnam Medical Journal ; : 145-150, 2016.
Article in English | WPRIM | ID: wpr-25334

ABSTRACT

¹²³I-meta-iodobenzylguanidine (MIBG) has become widely applied in Japan since its introduction to clinical cardiology and neurology practice in the 1990s. Neurological studies found decreased cardiac uptake of ¹²³I-MIBG in Lewy-body diseases including Parkinson's disease and dementia with Lewy bodies. Thus, cardiac MIBG uptake is now considered a biomarker of Lewy body diseases. Although scintigraphic images of ¹²³I-MIBG can be visually interpreted, an average count ratio of heart-to-mediastinum (H/M) has commonly served as a semi-quantitative marker of sympathetic activity. Since H/M ratios significantly vary according to acquisition and processing conditions, quality control should be appropriate, and quantitation should be standardized. The threshold H/M ratio for differentiating Lewy-body disease is 2.0-2.1, and was based on standardized H/M ratios to comparable values of medium-energy collimators. Parkinson's disease can be separated from various types of parkinsonian syndromes using cardiac ¹²³I-MIBG, whereas activity is decreased on images of Lewy-body diseases using both ¹²³I-ioflupane for the striatum and ¹²³I-MIBG. Despite being a simple index, the H/M ratio of ¹²³I-MIBG uptake is reproducible and can serve as an effective tool to support a diagnosis of Lewy-body diseases in neurological practice.


Subject(s)
3-Iodobenzylguanidine , Cardiology , Dementia , Diagnosis , Japan , Lewy Bodies , Lewy Body Disease , Neurology , Nuclear Medicine , Parkinson Disease , Parkinsonian Disorders , Quality Control
17.
Rev. Kairós ; 18(4): 398-404, dez. 2015.
Article in Portuguese | LILACS | ID: biblio-986243

ABSTRACT

O presente trabalho é uma revisão bibliográfica com o objetivo de identificar e apresentar as produções científicas relacionadas à atuação da fisioterapia especificamente na Demência por Corpúsculos de Lewy (DCL). O critério de exclusão da pesquisa são estudos que tratam da atuação da fisioterapia na Doença de Alzheimer (DA) e na Doença de Parkinson (DP, que precede a síndrome demencial). Conclui-se que não existem estudos com resultados conclusivos sobre a atuação da fisioterapia na DCL


This study is a literature review in order to identify and present the scientific production related to the role of physiotherapy specifically in dementia by Lewy bodies. The search criterion for exclusion are the physiotherapy performance of studies in Alzheimer's disease and Parkinson's disease (which precedes dementia). It is concluded that there are insufficient studies for a possible review and discussion of the role of physiotherapy.


Subject(s)
Humans , Rehabilitation , Databases, Bibliographic , Lewy Bodies , Physical Therapy Specialty , Dementia , Chronic Disease
18.
Article in English | WPRIM | ID: wpr-203518

ABSTRACT

Pharmacological interventions are critical in dementia treatment to prevent disease progression. In this review, we aim to summarize and discuss about the current developments and recommendations in the pharmacological treatment of dementia. Cholinesterase inhibitors have demonstrated efficacy for Alzheimer's disease, mixed pathology with vascular dementia and Parkinson's disease dementia. The comparison study revealed no difference between each cholinesterase inhibitors. A high incidence of side effects of cholinesterase inhibitors could lower compliance. In this case, changing to the other drug or trying a transdermal type could be the solution. Memantine, a N-methyl-D-aspartate receptor antagonist, has proven to improve function at moderate to severe dementia and for dementia with Lewy body. But there are still insufficient evidences for the combination of a cholinesterase inhibitors and memantine. Discontinuing medicine in moderate to severe dementia may lead to worsening of cognitive function. For this reason, improving patients' compliance is important and for drug selection we should consider the type of dementia, severity of cognitive impairment and side effects of each medicine. Noncognitive symptoms, behavioral and psychological symptoms of dementia (BPSD) are common and can dominate disease presentation. For depression, selective serotonin reuptake inhibitors could be effective. Atypical antipsychotics could be used for other neuropsychological symptoms such as agitation, aggression, delusions and hallucinations.


Subject(s)
Aggression , Alzheimer Disease , Antipsychotic Agents , Behavioral Symptoms , Cholinesterase Inhibitors , Compliance , Delusions , Dementia , Dementia, Vascular , Depression , Dihydroergotamine , Disease Progression , Hallucinations , Incidence , Lewy Bodies , Memantine , N-Methylaspartate , Parkinson Disease , Pathology , Serotonin Uptake Inhibitors
19.
Experimental Neurobiology ; : 292-313, 2014.
Article in English | WPRIM | ID: wpr-113795

ABSTRACT

Alpha-synuclein is a small neuronal protein that is closely associated with the etiology of Parkinson's disease. Mutations in and alterations in expression levels of alpha-synuclein cause autosomal dominant early onset heredity forms of Parkinson's disease, and sporadic Parkinson's disease is defined in part by the presence of Lewy bodies and Lewy neurites that are composed primarily of alpha-synuclein deposited in an aggregated amyloid fibril state. The normal function of alpha-synuclein is poorly understood, and the precise mechanisms by which it leads to toxicity and cell death are also unclear. Although alpha-synuclein is a highly soluble, cytoplasmic protein, it binds to a variety of cellular membranes of different properties and compositions. These interactions are considered critical for at least some normal functions of alpha-synuclein, and may well play critical roles in both the aggregation of the protein and its mechanisms of toxicity. Here we review the known features of alpha-synuclein membrane interactions in the context of both the putative functions of the protein and of its pathological roles in disease.


Subject(s)
alpha-Synuclein , Amyloid , Cell Death , Cytoplasm , Heredity , Lewy Bodies , Membranes , Neurites , Neurons , Parkinson Disease , Synaptic Transmission
20.
Experimental Neurobiology ; : 337-344, 2014.
Article in English | WPRIM | ID: wpr-113792

ABSTRACT

Multiple system atrophy (MSA) is a rare, yet fatal neurodegenerative disease that presents clinically with autonomic failure in combination with parkinsonism or cerebellar ataxia. MSA impacts on the autonomic nervous system affecting blood pressure, heart rate and bladder function, and the motor system affecting balance and muscle movement. The cause of MSA is unknown, no definitive risk factors have been identified, and there is no cure or effective treatment. The definitive pathology of MSA is the presence of alpha-synuclein aggregates in the brain and therefore MSA is classified as an alpha-synucleinopathy, together with Parkinson's disease and dementia with Lewy bodies. Although the molecular mechanisms of misfolding, fibrillation and aggregation of alpha-synuclein partly overlap with other alpha-synucleinopathies, the pathological pathway of MSA is unique in that the principal site for alpha-synuclein deposition is in the oligodendrocytes rather than the neurons. The sequence of pathological events of MSA is now recognized as abnormal protein redistributions in oligodendrocytes first, followed by myelin dysfunction and then neurodegeneration. Oligodendrocytes are responsible for the production and maintenance of myelin, the specialized lipid membrane that encases the axons of all neurons in the brain. Myelin is composed of lipids and two prominent proteins, myelin basic protein and proteolipid protein. In vitro studies suggest that aberration in protein distribution and lipid transport may lead to myelin dysfunction in MSA. The purpose of this perspective is to bring together available evidence to explore the potential role of alpha-synuclein, myelin protein dysfunction, lipid dyshomeostasis and ABCA8 in MSA pathogenesis.


Subject(s)
alpha-Synuclein , Autonomic Nervous System , Axons , Blood Pressure , Brain , Cerebellar Ataxia , Dementia , Heart Rate , Lewy Bodies , Membranes , Multiple System Atrophy , Myelin Proteins , Myelin Sheath , Neurodegenerative Diseases , Neurons , Oligodendroglia , Parkinson Disease , Parkinsonian Disorders , Pathology , Risk Factors , Urinary Bladder
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