Neuroimaging of Dementia with Lewy Bodies

2017 ◽  
pp. 221-231
Author(s):  
Haruo Hanyu
Keyword(s):  
Dementia With Lewy Bodies ◽  
Lewy Bodies

Differences in glucose metabolism between dementia with Lewy bodies and dementia associated with Parkinson's disease

2005 ◽  
Vol 32 (S 4) ◽  
Author(s):  
P Häussermann ◽  
A.O Ceballos-Baumann ◽  
H Förstl ◽  
R Feurer ◽  
B Conrad ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Glucose Metabolism ◽  
Dementia With Lewy Bodies ◽  
Lewy Bodies

Dementia with Lewy bodies

2018 ◽  
pp. 11-21
Author(s):  
O. S. Levin ◽  
E. E. Vasenina ◽  
A. Sh. Chimagomedova ◽  
N. G. Dudchenko
Keyword(s):  
Parkinson’S Disease ◽  
Dementia With Lewy Bodies ◽  
Cholinesterase Inhibitors ◽  
Lewy Bodies ◽  
Diagnosis And Treatment ◽  
Modern Concept ◽  
Historical Aspect ◽  
Neurodegenerative Process ◽  
Icd 10

Te lecture presents modern concept of the symptoms, diagnosis and treatment of dementia with Lewy bodies (DLB), which accounts for about 10% of cases of dementia. Te nosological status of DLB and the problem of ratio of DLB and Parkinson’s disease which, apparently, represent two phenotypic variants of one neurodegenerative process («diseases with Lewy bodies») are considered in historical aspect. Approaches to the diagnosis and coding of DLB in accordance with ICD-10 are proposed. Te role of cholinesterase inhibitors, antipsychotics, levodopa, rasagiline and other drugs in the treatment of patients with DLB is аnalyzed.

Dementia with Lewy bodies—associated ß-synuclein mutations V70M and P123H cause mutation-specific neuropathological lesions

2021 ◽  
Author(s):  
Maryna Psol ◽  
Sofia Guerin Darvas ◽  
Kristian Leite ◽  
Sameehan U Mahajani ◽  
Mathias Bähr ◽  
...  
Keyword(s):  
Neuronal Network ◽  
Dementia With Lewy Bodies ◽  
Lewy Bodies ◽  
Sporadic Case ◽  
Network Activity ◽  
Proteinase K ◽  
Neuronal Network Activity ◽  
Distinct Disease

Abstract ß-Synuclein (ß-Syn) has long been considered to be an attenuator for the neuropathological effects caused by the Parkinson’s disease-related α-Synuclein (α-Syn) protein. However, recent studies demonstrated that overabundant ß-Syn can form aggregates and induce neurodegeneration in CNS neurons in vitro and in vivo, albeit at a slower pace as compared to α-Syn. Here we demonstrate that ß-Syn mutants V70M, detected in a sporadic case of Dementia with Lewy Bodies (DLB), and P123H, detected in a familial case of DLB, robustly aggravate the neurotoxic potential of ß-Syn. Intriguingly, the two mutations trigger mutually exclusive pathways. ß-Syn V70M enhances morphological mitochondrial deterioration and degeneration of dopaminergic and non-dopaminergic neurons, but has no influence on neuronal network activity. Conversely, ß-Syn P123H silences neuronal network activity, but does not aggravate neurodegeneration. ß-Syn WT, V70M and P123H formed proteinase K (PK) resistant intracellular fibrils within neurons, albeit with less stable C-termini as compared to α-Syn. Under cell free conditions, ß-Syn V70M demonstrated a much slower pace of fibril formation as compared to WT ß-Syn, and P123H fibrils present with a unique phenotype characterized by large numbers of short, truncated fibrils. Thus, it is possible that V70M and P123H cause structural alterations in ß-Syn, that are linked to their distinct neuropathological profiles. The extent of the lesions caused by these neuropathological profiles is almost identical to that of overabundant α-Syn, and thus likely to be directly involved into etiology of DLB. Over all, this study provides insights into distinct disease mechanisms caused by mutations of ß-Syn.

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