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1 midbrain containing dopaminergic neurons and neuromelanin.
2 ons store iron in the form of ferrous ion or neuromelanin.
3 -1451, such as neuronal monoamine oxidase or neuromelanin.
4 levels of the dopamine-derived brain pigment neuromelanin.
5  derivatives that may serve as precursors to neuromelanin.
6 tantia nigra tissue and in various synthetic neuromelanins.
7 cluding dopamine-specific phenotypes such as neuromelanin accumulation.
8         [F-18]-AV-1451 off-target binding to neuromelanin- and melanin-containing cells and, to a les
9 ghtly different in the natural and synthetic neuromelanin, are both approximately 2.0 A.
10 ; a finding similar to our earlier report in neuromelanin cells from the substantia nigra of restless
11 D, not disease duration, whereas the loss of neuromelanin cells is significantly correlated only with
12 tionship of similar strength between loss of neuromelanin containing cells and the clinical symptoms
13  = 0.0006, t = 4.25, df = 15) in the size of neuromelanin containing cells in PD patients, but no dif
14 us and correlated positively with numbers of neuromelanin-containing (noradrenergic) cells along the
15 s coeruleus, paralleling an uneven number of neuromelanin-containing (noradrenergic) neurons througho
16 t negative correlation between the number of neuromelanin-containing cells at a given level and age (
17 ralleled by a similar uneven distribution of neuromelanin-containing cells in both major depressives
18 of DAT-containing neurons to total number of neuromelanin-containing cells in each subject's sample.
19 tem histochemical staining showed absence of neuromelanin-containing cells in the basal ganglia, indi
20  2-adrenoceptors coordinately with counts of neuromelanin-containing cells in tissue sections cryocut
21 ignificant correlation between the number of neuromelanin-containing cells per section and the specif
22 ration of binding and the greatest number of neuromelanin-containing cells per section occurred near
23  Both the binding of [125I]PIC and number of neuromelanin-containing cells were differentially distri
24 auses that produce massive cell death of the neuromelanin-containing dopaminergic neurons of the subs
25 tal age-related neurofibrillary tangles) and neuromelanin-containing neurons in the substantia nigra
26 mined, expression was highly elevated within neuromelanin-containing neurons of the substantia nigra
27 n the midbrain, AKR7A2 was found in glia and neuromelanin-containing neurons of the substantia nigra,
28 ignificant correlation between the number of neuromelanin-containing neurons per section and the spec
29 he 35% and 41% reductions in total number of neuromelanin-containing neurons seen in middle-aged and
30 htly stained; and type 3, DAT-immunonegative neuromelanin-containing perikarya.
31 us ceruleus neurons were identified by their neuromelanin content.
32 ironment of the iron site in natural (human) neuromelanin extracted from substantia nigra tissue and
33                                              Neuromelanin granules are yet only partially characteris
34 first time to isolate a sufficient amount of neuromelanin granules for global proteomics analysis fro
35 viously published global proteome studies of neuromelanin granules in human substantia nigra required
36             To clarify the exact function of neuromelanin granules in humans, their enrichment and in
37 ribed findings, supporting the connection of neuromelanin granules to iron homeostasis and lysosomes
38 000 proteins were identified associated with neuromelanin granules.
39 pecific enrichment and proteomic analysis of neuromelanin granules.
40 ectrometry for the isolation and analysis of neuromelanin granules.
41 phy to visualize the concentration of nigral neuromelanin in Parkinson's disease and correlated the f
42 e ligand (18)F-AV-1451 ((18)F-T807) binds to neuromelanin in the midbrain, and may therefore be a mea
43                                              Neuromelanin is a complex polymer pigment found primaril
44 nglia, indicating that off-target binding to neuromelanin is an insufficient explanation of 18F-AV-14
45 mbryonic stem cells, our human MLOs produced neuromelanin-like granules that were structurally simila
46                        Conclusion PD-induced neuromelanin loss can be quantified across imaging proto
47 ine hydroxylase immunoreactivity (TH-ir) and neuromelanin (NM) content revealed no difference in cell
48                                 In contrast, neuromelanin (NM) is found in deep brain regions, specif
49                                              Neuromelanin (NM) isolated from the substantia nigra reg
50 ive o-quinone species that are precursors of neuromelanin (NM) pigment and under pathological conditi
51 e initiation of melanoma, whereas, increased neuromelanin (NM), the melanin synthesized in dopaminerg
52 factors released from microglia activated by neuromelanin or alpha-synuclein, or high cytosolic DA an
53 n inverse relationship between VMAT2 ISI and neuromelanin pigment in the N1 and III neurons; 3) there
54                  In vitro data indicate that neuromelanin pigment is formed from the excess cytosolic
55                                              Neuromelanin pigment is stored in granules including a p
56 rea (VTA) of humans and mice by using either neuromelanin pigment or immunolabeling with tyrosine hyd
57 l SN neurons also contain significantly more neuromelanin pigment than the dopaminergic neurons in th
58 t the ventral SN neurons accumulate the most neuromelanin pigment, in part because they have the leas
59 in neurons that contain different amounts of neuromelanin pigment.
60 and 7 normal brains were used for a study of neuromelanin pigmented cell loss.
61 ce to the depigmentation and degeneration of neuromelanin-pigmented noradrenergic cell bodies in the
62    We find that ATF4 levels are increased in neuromelanin-positive neurons in the substantia nigra of
63                                              Neuromelanin-related volumes of the anterior and posteri
64 ation of hemosiderin (posterior portion) and neuromelanin (remainder).
65  30 control subjects) were investigated with neuromelanin-sensitive MR imaging by using two different
66        Purpose To investigate the pattern of neuromelanin signal intensity loss within the substantia
67 ins (such as amyloid-beta peptide [Abeta] or neuromelanin) that lead to oxidative stress have emerged
68              Results Reduction of normalized neuromelanin volume in PD was most pronounced in the pos
69                                   Normalized neuromelanin volume loss of the posterior and whole SNpc
70                                   Normalized neuromelanin volume of the anterior, posterior, and whol
71    Diagnostic test performance of normalized neuromelanin volume was investigated by using receiver o
72 gmental area were determined, and normalized neuromelanin volumes were assessed for protocol-dependen

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