scholarly journals Lafora and Trétiakoff: the naming of the inclusion bodies discovered by Lewy

2017 ◽  
Vol 75 (10) ◽  
pp. 751-753 ◽  
Author(s):  
Eliasz Engelhardt
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Substantia Nigra ◽  
Inclusion Bodies ◽  
Lewy Bodies ◽  
Brain Nuclei ◽  
Paralysis Agitans ◽  
One Year ◽  
First Time

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.

Leopold Ordenstein: on paralysis agitans and multiple sclerosis

2007 ◽  
Vol 13 (9) ◽  
pp. 1195-1199 ◽  
Author(s):  
H.C. Lehmann ◽  
H.-P. Hartung ◽  
B.C. Kieseier
Keyword(s):  
Multiple Sclerosis ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
French Language ◽  
Doctoral Thesis ◽  
Paralysis Agitans ◽  
History Of ◽  
First Time ◽  
Jean Martin Charcot

In 1868 the German Leopold Ordenstein (1835—1902) published in Paris a doctoral thesis in French language under the patronage of Jean-Martin Charcot (1825—1893). For the first time, multiple sclerosis and Parkinson's disease were clearly recognized as different clinical entities, based on clinical and pathological data. Ordenstein's work represents today a fundamental and often credited, yet still widely unknown, contribution to the history of these two diseases. The present paper delivers a synopsis of this key document. In addition, the life and work of Leopold Ordenstein will be reviewed. Multiple Sclerosis 2007; 13: 1195—1199. http://msj.sagepub.com

scholarly journals Interaction between coxsackievirus B3 infection and α-synuclein in models of Parkinson’s disease

2021 ◽  
Vol 17 (10) ◽  
pp. e1010018
Author(s):  
Soo Jin Park ◽  
Uram Jin ◽  
Sang Myun Park
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Inclusion Body ◽  
Dopaminergic Neurons ◽  
Inclusion Bodies ◽  
Lewy Bodies ◽  
Coxsackievirus B3 ◽  
Body Formation ◽  
Inclusion Body Formation ◽  
Cvb3 Infection

Parkinson’s disease (PD) is one of the most common neurodegenerative diseases. PD is pathologically characterized by the death of midbrain dopaminergic neurons and the accumulation of intracellular protein inclusions called Lewy bodies or Lewy neurites. The major component of Lewy bodies is α-synuclein (α-syn). Prion-like propagation of α-syn has emerged as a novel mechanism in the progression of PD. This mechanism has been investigated to reveal factors that initiate Lewy pathology with the aim of preventing further progression of PD. Here, we demonstrate that coxsackievirus B3 (CVB3) infection can induce α-syn-associated inclusion body formation in neurons which might act as a trigger for PD. The inclusion bodies contained clustered organelles, including damaged mitochondria with α-syn fibrils. α-Syn overexpression accelerated inclusion body formation and induced more concentric inclusion bodies. In CVB3-infected mice brains, α-syn aggregates were observed in the cell body of midbrain neurons. Additionally, α-syn overexpression favored CVB3 replication and related cytotoxicity. α-Syn transgenic mice had a low survival rate, enhanced CVB3 replication, and exhibited neuronal cell death, including that of dopaminergic neurons in the substantia nigra. These results may be attributed to distinct autophagy-related pathways engaged by CVB3 and α-syn. This study elucidated the mechanism of Lewy body formation and the pathogenesis of PD associated with CVB3 infection.

scholarly journals Pesticides and Parkinson’s Disease

2001 ◽  
Vol 1 ◽  
pp. 207-208 ◽  
Author(s):  
Todd B. Sherer ◽  
Ranjita Betarbet ◽  
J. Timothy Greenamyre
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Substantia Nigra ◽  
Neurodegenerative Disorder ◽  
Late Onset ◽  
Lewy Bodies ◽  
Substantia Nigra Pars Compacta ◽  
Selective Death ◽  
Underlying Mechanisms ◽  
Common Neurodegenerative Disorder

Parkinson’s disease (PD), a common neurodegenerative disorder affects approximately 1% of the population over 65. PD is a late-onset progressive motor disease characterized by tremor, rigidity (stiffness), and bradykinesia (slowness of movement). The hallmark of PD is the selective death of dopamine-containing neurons in the substantia nigra pars compacta which send their projections to the striatum and the presence of cytoplasmic aggregates called Lewy bodies [1-2]. Most cases of PD are sporadic but rare cases are familial, with earlier onset. The underlying mechanisms and causes of PD still remain unclear.

scholarly journals Progress in Clinical Neurosciences: Parkinson's Disease with Dementia and Dementia with Lewy Bodies

2004 ◽  
Vol 31 (1) ◽  
pp. 7-21 ◽  
Author(s):  
Richard Camicioli ◽  
Nancy Fisher
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Lewy Body ◽  
Dementia With Lewy Bodies ◽  
Lewy Bodies ◽  
Imaging Findings ◽  
Functional Impact ◽  
Assessment And Treatment ◽  
Parkinson’S Disease With Dementia ◽  
One Year

Dementia occurs in up to 30% of people with Parkinson's disease and is a major cause of disability. Pathologically, Parkinson's dementia, where dementia follows the onset of parkinsonism by at least one year, overlaps with dementia with Lewy bodies. We review the functional impact, definitions, neuropsychology, epidemiology and pathophysiology of Parkinson's dementia, dementia with Lewy bodies and their overlap. Associated psychiatric and imaging findings are also considered. Lastly, current and emerging approaches to assessment and treatment in patients with these Lewy body associated dementias are presented.

scholarly journals Lewy and his inclusion bodies: Discovery and rejection

2017 ◽  
Vol 11 (2) ◽  
pp. 198-201 ◽  
Author(s):  
Eliasz Engelhardt ◽  
Marleide da Mota Gomes
Keyword(s):  
Parkinson Disease ◽  
Lewy Body ◽  
Inclusion Bodies ◽  
Lewy Bodies ◽  
Brain Nuclei ◽  
Eosinophilic Inclusion ◽  
Paralysis Agitans ◽  
Extensive Information ◽  
The Subject ◽  
Lewy Body Diseases

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.

scholarly journals [18F]-AV-1451 binding in the substantia nigra as a marker of neuromelanin in lewy body diseases

2021 ◽  
Author(s):  
Elijah Mak ◽  
Antonina Kouli ◽  
Negin Holland ◽  
Nicolas Nicastro ◽  
George Savulich ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Substantia Nigra ◽  
Lewy Body ◽  
Dementia With Lewy Bodies ◽  
Disease Duration ◽  
Rating Scale ◽  
Surrogate Marker ◽  
Lewy Bodies ◽  
Lewy Body Diseases

Abstract While [18F]-AV-1451 was developed as a positron emission tomography (PET) radiotracer with high affinity for hyperphosphorylated tau, it has been proposed that loss of “off-target” [18F]-AV-1451 binding to neuromelanin in the substantia nigra could be a surrogate marker of Lewy body diseases. [18F]-AV-1451 binding was measured in the substantia nigra of patients with Parkinson’s disease (n = 35), dementia with Lewy bodies (n = 10) and separate control groups (n = 37; n = 14). Associations with motor symptoms, cognition, and disease duration were evaluated using linear regression models. The dementia with Lewy bodies group had significantly reduced substantia nigra [18F]-AV-1451 binding compared to controls after adjusting for age (p < 0.05). However, there were no significant differences in substantia nigra [18F]-AV-1451 binding between Parkinson’s disease and controls. Substantia nigra [18F]-AV-1451 binding was not associated with age, disease duration, Movement Disorders Society—Unified Parkinson’s Disease Rating Scale and cognitive scores in dementia with Lewy bodies and Parkinson’s disease groups. Despite the reduction of substantia nigra [18F]-AV-1451 binding in dementia with Lewy bodies, these findings suggest that substantia nigra [18F]-AV-1451 binding has no value as a diagnostic marker in early Parkinson’s disease. Further investigations in longitudinal cohorts are warranted.

scholarly journals A/T/(N) Profile in Cerebrospinal Fluid of Parkinson’s Disease with/without Cognitive Impairment and Dementia with Lewy Bodies

Diagnostics ◽  
2020 ◽  
Vol 10 (12) ◽  
pp. 1015
Author(s):  
Giovanni Bellomo ◽  
Federico Paolini Paoletti ◽  
Elena Chipi ◽  
Maya Petricciuolo ◽  
Simone Simoni ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cerebrospinal Fluid ◽  
Cognitive Impairment ◽  
Dementia With Lewy Bodies ◽  
Lewy Bodies ◽  
Amyloid Plaques ◽  
Phosphorylated Tau ◽  
Total Tau ◽  
One Year

Neuropathological investigations report that in synucleinopathies with dementia, namely Parkinson’s disease (PD) with dementia (PDD) and dementia with Lewy bodies (DLB), the histopathological hallmarks of Alzheimer’s Disease (AD), in particular amyloid plaques, are frequently observed. In this study, we investigated the cerebrospinal fluid (CSF) AD biomarkers in different clinical phenotypes of synucleinopathies. CSF Aβ42/Aβ40 ratio, phosphorylated tau and total tau were measured as markers of amyloidosis (A), tauopathy (T) and neurodegeneration (N) respectively, in 98 PD (48 with mild cognitive impairment, PD-MCI; 50 cognitively unimpaired, PD-nMCI), 14 PDD and 15 DLB patients, and 48 neurological controls (CTRL). In our study, CSF AD biomarkers did not significantly differ between CTRL, PD-MCI and PD-nMCI patients. In PD-nMCI and PD-MCI groups, A-/T-/N- profile was the most represented. Prevalence of A+ was similar in PD-nMCI and PD-MCI (10% and 13%, respectively), being higher in PDD (64%) and in DLB (73%). DLB showed the lowest values of Aβ42/Aβ40 ratio. Higher total tau at baseline predicted a worse neuropsychological outcome after one year in PD-MCI. A+/T+, i.e., AD-like CSF profile, was most frequent in the DLB group (40% vs. 29% in PDD).

scholarly journals MicroRNAs: Game Changers in the Regulation of α-Synuclein in Parkinson’s Disease

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Liang Zhao ◽  
Zhiqin Wang
Keyword(s):  
Gene Expression ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Substantia Nigra ◽  
Neurodegenerative Disorder ◽  
Noncoding Rnas ◽  
Lewy Bodies ◽  
Neuronal Loss ◽  
Substantia Nigra Pars Compacta ◽  
Common Neurodegenerative Disorder

Parkinson’s disease (PD) is the second most common neurodegenerative disorder. Its neuropathological hallmarks include neuronal loss in the substantia nigra pars compacta (SNpc) and the presence of Lewy bodies containing aggregates of α-synuclein (α-syn). An imbalance between the rates of α-syn synthesis, aggregation, and clearance can result in abnormal α-syn levels and contribute to the pathogenesis of PD. MicroRNAs (miRNAs) are endogenous single-stranded noncoding RNAs (∼22 nucleotides) that have recently emerged as key posttranscriptional regulators of gene expression. In this review, we summarize the functions of miRNAs that directly target α-syn. We also review miRNAs that indirectly impact α-syn levels or toxicity through different pathways, including those involved in the clearance of α-syn and neuroinflammation.

scholarly journals The gut-brain axis in the pathogenesis of Parkinson’s disease

2019 ◽  
Vol 5 (2) ◽  
pp. 73-81 ◽  
Author(s):  
Lanxia Meng ◽  
Xin Yuan ◽  
Xuebing Cao ◽  
Zhentao Zhang
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Nervous System ◽  
Substantia Nigra ◽  
Enteric Nervous System ◽  
Lewy Bodies ◽  
Motor Symptoms ◽  
Gastrointestinal Dysfunction ◽  
Neurodegenerative Process ◽  
The Central Nervous System

Parkinson’s disease (PD) is the second most common neurodegenerative disease. Its pathological markers include Lewy bodies and Lewy neuritis, which primarily affect the substantia nigra. However, in recent years, mounting evidence suggests that PD is a multifocal neurodegenerative process that influences several neuronal structures aside from the substantia nigra, one of which is the enteric nervous system. Many clinical studies have reported that patients with PD experience gastrointestinal dysfunction for many years before the onset of motor symptoms. Emerging evidence indicates that α-synuclein deposition may start in the enteric nervous system and then propagate to the central nervous system. The gut-brain axis plays an important role in PD pathogenesis. Recent evidence suggests that these interactions may be primarily affected by the intestinal microbiota. In this review, the authors discuss recent research, and illustrate how changes in the composition of the gut microbiota may trigger inflammation, thus contributing to neurodegeneration in PD.

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