We are analyzing https://link.springer.com/article/10.1007/s12035-012-8280-y.

Title:
The Lewy Body in Parkinson’s Disease and Related Neurodegenerative Disorders | Molecular Neurobiology
Description:
The histopathological hallmark of Parkinson’s disease (PD) is the presence of fibrillar aggregates referred to as Lewy bodies (LBs), in which α-synuclein is a major constituent. Pale bodies, the precursors of LBs, may serve the material for that LBs continue to expand. LBs consist of a heterogeneous mixture of more than 90 molecules, including PD-linked gene products (α-synuclein, DJ-1, LRRK2, parkin, and PINK-1), mitochondria-related proteins, and molecules implicated in the ubiquitin–proteasome system, autophagy, and aggresome formation. LB formation has been considered to be a marker for neuronal degeneration because neuronal loss is found in the predilection sites for LBs. However, recent studies have indicated that nonfibrillar α-synuclein is cytotoxic and that fibrillar aggregates of α-synuclein (LBs and pale bodies) may represent a cytoprotective mechanism in PD.
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Keywords {🔍}

google, scholar, article, pubmed, cas, lewy, disease, bodies, parkinsons, neuropathol, αsynuclein, body, acta, brain, neurol, protein, wakabayashi, inclusions, takahashi, mori, pathol, dementia, exp, pathology, neurosci, system, neuronal, human, res, parkinson, neurobiol, lett, neurodegenerative, disorders, tanji, brains, formation, accumulation, glial, neurons, biol, mol, kakita, chem, research, ann, braak, cortical, neuropathology, immunoreactivity,

Topics {✒️}

adult-onset hallervorden–spatz disease c-terminal alpha-synuclein immunoreactivity nacp/α-synuclein-positive filamentous inclusions proteinase k-resistant α-synuclein α-synuclein/nacp-immunoreactive neuronal inclusions month download article/chapter glycogen synthase kinase-3beta lewy body-related α-synucleinopathy cu/zn superoxide dismutase ubiquitin carboxyl-terminal hydrolase synaptic vesicle-specific protein gene encoding α-synuclein α-synuclein gene identified prolyl-isomerase pin1 accumulates agrin binds α-synuclein modulates α-synuclein fibrillation α-synuclein locus triplication gene encoding omi/htra2 tissue transglutaminase-induced aggregation binds α-synuclein filaments lewy body-type degeneration premature α-synuclein aggregates aminoacyl-trna synthetase complex tppp/p25 protein nacp/α-synuclein immunoreactivity olfactory bulb α-synucleinopathy phosphorylated α-synuclein histopathology a30p mutant alpha-synuclein lewy body-bearing neurons phosphorylated α-synuclein immunoreactivity beta-amyloid precursor proteins full article pdf tau-negative glial inclusions cyclin-dependent kinase 5 annular α-synuclein protofibrils amyotrophic lateral sclerosis phospholipase c-δ brainstem-type lewy bodies disease-related brain pathology privacy choices/manage cookies misfolded protein stress nacp/α-synuclein α-synuclein/nacp ca2–3 neurites specific autonomic nervous system peripheral nervous system α-synuclein aggregation α-synuclein aggregates autonomic nervous systems aggresome-related protein

Questions {❓}

Braak H, Müller CM, Rüb U et al (2006) Pathology associated with sporadic Parkinson’s disease-where does it end?
Minguez-Castellanos A, Chamorro CE, Escamilla-Sevilla F et al (2007) Do α-synuclein aggregates in autonomic plexuses predate Lewy body disorders?
Münch G, Lüth HJ, Wong A et al (2000) Crosslinking of α-synuclein by advanced glycation endproducts—an early pathophysiological step in Lewy body formation?
Reverse engineering Lewy bodies: how far have we come and how far can we go?
Sidhu A, Wersinger C, Vernier P (2004) Does α-synuclein modulate dopaminergic synaptic content and tone at the synapse?
Terry RD (2000) Do neuronal inclusions kill the cell?

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