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1 in the presence of ubiquitin-positive, intra-neuronal inclusions.
2 tients have ubiquitin-positive, tau-negative neuronal inclusions.
3 d is colocalized in ALS-affected spinal cord neuronal inclusions.
4 h the accumulation of dynein and dynactin in neuronal inclusions.
5 S patients and colocalize with ubiquitinated neuronal inclusions.
6 et disease brains contain ubiquitin-positive neuronal inclusions, a pathologic hallmark of protein-me
7                                              Neuronal inclusions also have been reported but remain l
8                                              Neuronal inclusions also were identified in regions not
9 th citalopram significantly reduced ataxin 3 neuronal inclusions and astrogliosis, rescued diminished
10 peptides that accumulate within intranuclear neuronal inclusions and contribute to neurotoxicity.
11 ing and accumulation of misfolded protein in neuronal inclusions and plaques.
12 , the skin-amplified alphaSyn strains induce neuronal inclusions and trigger degeneration of induced
13 aptic and synaptic NMDAR activity, decreases neuronal inclusions and worsens these outcomes.
14 , hyperphosphorylated cytoskeletal proteins, neuronal inclusions, and neurodegeneration, that are com
15 inherited dementia, histologically by unique neuronal inclusion bodies and biochemically by polymers
16 racellular protein aggregates reminiscent of neuronal inclusion bodies and caused more cancer cell de
17  key pathological finding is the presence of neuronal inclusion bodies distributed throughout the gra
18 lial dementias, but whether the formation of neuronal inclusion bodies is a causative or incidental f
19 ant protein, this neurodegeneration exhibits neuronal inclusion bodies that are Hsp70 and ubiquitin p
20 mine tract, forms fibrils that accumulate in neuronal inclusion bodies, resulting in Huntington's dis
21 e tract, form fibrils that accumulate within neuronal inclusion bodies, resulting in the fatal neurod
22 mulation of ubiquitin (Ub) conjugates within neuronal inclusion bodies.
23 es, and in the nucleus, forming intranuclear neuronal inclusion bodies.
24 gation and have broad implications for other neuronal inclusion body diseases.
25 es of ubiquitinated proteins are detected in neuronal inclusions, but their role in neurodegeneration
26 y is characterized by the formation of intra-neuronal inclusions called Lewy bodies, which are compri
27 ng a mutated huntingtin fragment demonstrate neuronal inclusions, characteristic neuropathology, and
28 nerative disorder characterized by fibrillar neuronal inclusions composed of aggregated alpha-synucle
29                                              Neuronal inclusions composed of the exon 1 protein and u
30 distinct molecular actions as TDP-43 and FUS neuronal inclusions do not overlap, with FUS inclusions
31  tract degeneration, gliosis and cytoplasmic neuronal inclusions formed by TDP-43 or TAR DNA binding
32 omprising beta-amyloid (Abeta) peptides, and neuronal inclusions formed from tau protein.
33 uman TDP-43 represents the main component of neuronal inclusions found in patients with neurodegenera
34 s with neurodegenerative disease and typical neuronal inclusions had biopsy or autopsy material avail
35 eral sclerosis and fused in sarcoma-positive neuronal inclusions have subsequently been demonstrated
36 aggregates formed in cultured cells and into neuronal inclusions in a transgenic mouse model of FUSop
37 bination of memory impairment developed more neuronal inclusions in the dentate gyrus, cornu ammonis
38 finding was the identification of widespread neuronal inclusions in the majority of patients, not onl
39 ent near the injection site, we found mainly neuronal inclusions in the remote brain area, consistent
40 hologic type, topography, and frequencies of neuronal inclusions, including globular cytoplasmic (Lew
41 on of alpha-synuclein (alpha-syn) fibrils in neuronal inclusions is the defining pathological process
42 diseases, the mutant protein aggregates into neuronal inclusions; it is generally, although not unive
43 ized by abundant alpha-synuclein (alpha-Syn) neuronal inclusions, known as Lewy bodies and Lewy neuri
44 lein is a primary component of the fibrillar neuronal inclusions, known as Lewy bodies, that are diag
45 ncreases in the proportion of microglia with neuronal inclusions, limited dendritic spine loss in the
46 alpha-synuclein (alphasyn) as opposed to the neuronal inclusions more commonly found in other alpha-s
47 xtends survival and delays the appearance of neuronal inclusions, neurotransmitter receptor alteratio
48 mponent of the Lewy body, the characteristic neuronal inclusion of the Parkinson's disease (PD) brain
49                                              Neuronal inclusions of aggregated RNA-binding protein fu
50                                              Neuronal inclusions of hyperphosphorylated and aggregate
51                                              Neuronal inclusions of poly(GA), a protein unconventiona
52       The pathological hallmarks of FTLD are neuronal inclusions of specific, abnormally assembled pr
53                    However, the discovery of neuronal inclusions of TDP-43 as the neuropathological h
54       Frontotemporal lobar degeneration with neuronal inclusions of the TAR DNA-binding protein 43 (F
55                                              Neuronal inclusion pathology appeared to follow a hierar
56 mentia with tau-negative, ubiquitin-positive neuronal inclusion pathology.
57 acterized by ubiquitin-positive intranuclear neuronal inclusions, raising the possibility that failur
58  degeneration (~45%) exhibit TDP-43 positive neuronal inclusions, suggesting a role for this protein
59 racterized pathologically by the presence of neuronal inclusions termed Lewy bodies (LBs).
60 cumulates, often in a ubiquitinated form, in neuronal inclusions termed Lewy bodies.
61 also had more alpha-synuclein-immunoreactive neuronal inclusions than alpha-synuclein singly tg mice.
62 rmation of toxic filamentous alpha-synuclein neuronal inclusions that cause neurodegeneration.
63  repeats, Gly-Arg, Pro-Arg, and Gly-Ala form neuronal inclusions that contain aggregates of the pepti
64      Like in many patients with FTD and ALS, neuronal inclusions that contain TARDBP are seen, but ar
65 3), the pathological diagnosis was FTLD with neuronal inclusions that contained TAR DNA-binding prote
66 insoluble material in brain homogenates, and neuronal inclusions throughout the CNS of c9FTD/ALS case
67 characteristically associated with insoluble neuronal inclusions, usually intranuclear, and neuronal
68 luding globular cytoplasmic (Lewy body-like) neuronal inclusions, were determined across a wide spect
69 y certain clinical symptoms and pathological neuronal inclusions with TAR DNA-binding protein (TDP-43
70                                 Argyrophilic neuronal inclusions, with a characteristic immunocytoche