The Role of α-Synuclein Assembly and Metabolism in the Pathogenesis of Lewy Body Disease

2004 ◽  
Vol 24 (3) ◽  
pp. 343-352 ◽  
Author(s):  
Makoto Hashimoto ◽  
Kohichi Kawahara ◽  
Pazit Bar-On ◽  
Edward Rockenstein ◽  
Leslie Crews ◽  
...  
Keyword(s):  
Lewy Body ◽  
Lewy Body Disease

The Role of 123I-Metaiodobenzylguanidine Myocardial Scintigraphy in the Diagnosis of Lewy Body Disease in Patients with Dementia in a Memory Clinic

2006 ◽  
Vol 22 (5-6) ◽  
pp. 379-384 ◽  
Author(s):  
Haruo Hanyu ◽  
Soichiro Shimizu ◽  
Kentaro Hirao ◽  
Hirofumi Sakurai ◽  
Toshihiko Iwamoto ◽  
...  
Keyword(s):  
Lewy Body ◽  
Lewy Body Disease ◽  
Myocardial Scintigraphy ◽  
Memory Clinic

The Vanishing Plaque

2001 ◽  
Vol 13 (1) ◽  
pp. 3-3 ◽  
Author(s):  
Robin Eastwood
Keyword(s):  
Risk Factors ◽  
Transgenic Mice ◽  
Lewy Body ◽  
Lewy Body Disease ◽  
Amyloid Plaques ◽  
Vascular Risk ◽  
Postmortem Diagnosis ◽  
Intelligence Education ◽  
Small Parts

Recently articles have appeared suggesting that in transgenic mice, vaccination with small parts of beta-amyloid can produce antibodies that prevent formation of amyloid plaques in the young and banishment in older mice. (Mice do not have tangles.) Because vaccines have eliminated or mitigated the effect of smallpox, polio, tuberculosis, and other dread diseases, such news is electrifying. However, disbelief is not long suspended when certain facts are presented. First, the role of plaques and tangles is moot. Second, there are reckoned to be at least 55 kinds of dementia, with Alzheimer's disease (AD) having a major but decreasing proportion as new types are recognized. (Thus some would argue that Lewy body disease constitutes as much as 20% of all dementias.) Third, AD is not well diagnosed in life, being a postmortem diagnosis. Finally, we now recognize that there is a considerable overlap between AD and vascular dementia in terms of etiobgy and presentation. So just what are we vaccinating against? Beyond that of course is the mixed bag of variables involved in AD. Think of age, gender, race, intelligence, education, aluminum, oxidants, cholinesterase, and vascular risk factors. These are but a few.

scholarly journals Complementary Role of 18F-FDG PET and 123I-Ioflupane SPECT in the Diagnosis of Lewy Body Disease

2014 ◽  
Vol 42 (3) ◽  
pp. 233-234
Author(s):  
P. Jolepalem ◽  
H. R. Balon ◽  
C.-Y. O. Wong ◽  
D. Wu
Keyword(s):  
Fdg Pet ◽  
Lewy Body ◽  
Lewy Body Disease ◽  
Complementary Role ◽  
18F Fdg

scholarly journals A Review of the Role of Anticholinergic Activity in Lewy Body Disease and Delirium

2015 ◽  
Vol 15 (3) ◽  
pp. 162-167 ◽  
Author(s):  
Yuka Kitajima ◽  
Koji Hori ◽  
Kimiko Konishi ◽  
Masayuki Tani ◽  
Hiroi Tomioka ◽  
...  
Keyword(s):  
Lewy Body ◽  
Lewy Body Disease ◽  
Anticholinergic Activity

scholarly journals Lewy body disease or diseases with Lewy bodies?

2022 ◽  
Vol 8 (1) ◽  
Author(s):  
Kateřina Menšíková ◽  
Radoslav Matěj ◽  
Carlo Colosimo ◽  
Raymond Rosales ◽  
Lucie Tučková ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Lewy Body ◽  
Molecular Genetic ◽  
Lewy Bodies ◽  
Lewy Body Disease ◽  
Selective Vulnerability ◽  
True Nature ◽  
Molecular Genetic Data

AbstractThe current nosological concept of α-synucleinopathies characterized by the presence of Lewy bodies (LBs) includes Parkinson’s disease (PD), Parkinson’s disease dementia (PDD), and dementia with Lewy bodies (DLB), for which the term “Lewy body disease” (LBD) has recently been proposed due to their considerable clinical and pathological overlap. However, even this term does not seem to describe the true nature of this group of diseases. The subsequent discoveries of α-synuclein (αSyn), SNCA gene, and the introduction of new immunohistochemical methods have started intensive research into the molecular-biological aspects of these diseases. In light of today’s knowledge, the role of LBs in the pathogenesis and classification of these nosological entities remains somewhat uncertain. An increasingly more important role is attributed to other factors as the presence of various LBs precursors, post-translational αSyn modifications, various αSyn strains, the deposition of other pathological proteins (particularly β-amyloid), and the discovery of selective vulnerability of specific cells due to anatomical configuration or synaptic dysfunction. Resulting genetic inputs can undoubtedly be considered as the main essence of these factors. Molecular–genetic data indicate that not only in PD but also in DLB, a unique genetic architecture can be ascertained, predisposing to the development of specific disease phenotypes. The presence of LBs thus remains only a kind of link between these disorders, and the term “diseases with Lewy bodies” therefore results somewhat more accurate.

scholarly journals Role of Cytochromecas a Stimulator of α-Synuclein Aggregation in Lewy Body Disease

1999 ◽  
Vol 274 (41) ◽  
pp. 28849-28852 ◽  
Author(s):  
Makoto Hashimoto ◽  
Ayako Takeda ◽  
Leigh J. Hsu ◽  
Takato Takenouchi ◽  
Eliezer Masliah
Keyword(s):  
Lewy Body ◽  
Lewy Body Disease

The role of NUB1 in α-synuclein degradation in Lewy body disease model mice

2016 ◽  
Vol 470 (3) ◽  
pp. 635-642 ◽  
Author(s):  
Kunikazu Tanji ◽  
Yasuo Miki ◽  
Atsushi Maruyama ◽  
Fumiaki Mori ◽  
Junsei Mimura ◽  
...  
Keyword(s):  
Lewy Body ◽  
Disease Model ◽  
Lewy Body Disease
Sign in / Sign up

Export Citation Format

Share Document