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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
9 th citalopram significantly reduced ataxin 3 neuronal inclusions and astrogliosis, rescued diminished
12 , hyperphosphorylated cytoskeletal proteins, neuronal inclusions, and neurodegeneration, that are com
13 inherited dementia, histologically by unique neuronal inclusion bodies and biochemically by polymers
14 racellular protein aggregates reminiscent of neuronal inclusion bodies and caused more cancer cell de
15 key pathological finding is the presence of neuronal inclusion bodies distributed throughout the gra
16 lial dementias, but whether the formation of neuronal inclusion bodies is a causative or incidental f
17 ant protein, this neurodegeneration exhibits neuronal inclusion bodies that are Hsp70 and ubiquitin p
21 es of ubiquitinated proteins are detected in neuronal inclusions, but their role in neurodegeneration
22 y is characterized by the formation of intra-neuronal inclusions called Lewy bodies, which are compri
23 ng a mutated huntingtin fragment demonstrate neuronal inclusions, characteristic neuropathology, and
25 distinct molecular actions as TDP-43 and FUS neuronal inclusions do not overlap, with FUS inclusions
26 tract degeneration, gliosis and cytoplasmic neuronal inclusions formed by TDP-43 or TAR DNA binding
27 uman TDP-43 represents the main component of neuronal inclusions found in patients with neurodegenera
28 s with neurodegenerative disease and typical neuronal inclusions had biopsy or autopsy material avail
29 eral sclerosis and fused in sarcoma-positive neuronal inclusions have subsequently been demonstrated
30 aggregates formed in cultured cells and into neuronal inclusions in a transgenic mouse model of FUSop
31 finding was the identification of widespread neuronal inclusions in the majority of patients, not onl
32 hologic type, topography, and frequencies of neuronal inclusions, including globular cytoplasmic (Lew
33 on of alpha-synuclein (alpha-syn) fibrils in neuronal inclusions is the defining pathological process
34 diseases, the mutant protein aggregates into neuronal inclusions; it is generally, although not unive
35 ized by abundant alpha-synuclein (alpha-Syn) neuronal inclusions, known as Lewy bodies and Lewy neuri
36 lein is a primary component of the fibrillar neuronal inclusions, known as Lewy bodies, that are diag
37 alpha-synuclein (alphasyn) as opposed to the neuronal inclusions more commonly found in other alpha-s
38 xtends survival and delays the appearance of neuronal inclusions, neurotransmitter receptor alteratio
39 mponent of the Lewy body, the characteristic neuronal inclusion of the Parkinson's disease (PD) brain
45 acterized by ubiquitin-positive intranuclear neuronal inclusions, raising the possibility that failur
48 also had more alpha-synuclein-immunoreactive neuronal inclusions than alpha-synuclein singly tg mice.
51 3), the pathological diagnosis was FTLD with neuronal inclusions that contained TAR DNA-binding prote
52 insoluble material in brain homogenates, and neuronal inclusions throughout the CNS of c9FTD/ALS case
53 characteristically associated with insoluble neuronal inclusions, usually intranuclear, and neuronal
54 luding globular cytoplasmic (Lewy body-like) neuronal inclusions, were determined across a wide spect
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