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1 ompaction, which is associated with worsened axonal pathology.
2 tions in cerebral white matter structure and axonal pathology.
3 ervous system but with additional peripheral axonal pathology.
4 in CMT disease primarily associated with an axonal pathology.
5 ures consistent with both motor neuronal and axonal pathology.
6 rotein (PLP) gene by oligodendrocytes causes axonal pathology.
7 ppear to be caused by the reduction of acute axonal pathology.
8 of substantia nigra dopaminergic neurons and axonal pathology, a cardinal pathological hallmark of PD
9 results demonstrate a pattern of widespread axonal pathology after lateral FP brain injury in the ra
10 ce of morphologically detectable synaptic or axonal pathology and again displayed regional selectivit
15 f EAE, with decreased demyelination, reduced axonal pathology, and decreased central nervous system (
18 he result of primary FMRP-deficiency-related axonal pathology, as opposed to secondary connectional d
19 acrophages, which is usually associated with axonal pathologies, astrocytes selectively remove large
25 may therefore represent one of the earliest axonal pathologies in SOD1(G93A) mice, which worsens at
29 Our findings point to a wider pattern of axonal pathology in bipolar disorder than previously tho
32 amyotrophic lateral sclerosis (ALS), display axonal pathologies including abnormal accumulations of p
36 al. report that the core motor phenotype and axonal pathology of HSPs are recapitulated in mice lacki
37 ociated with diminished dopamine release and axonal pathology of nigrostriatal dopaminergic projectio
38 e normal-appearing white matter reveal early axonal pathology outside inflammatory demyelinating lesi
39 d neurofilament compaction (NFC), two common axonal pathology processes involved in traumatic axonal
40 alpha-syn antibodies attenuated synaptic and axonal pathology, reduced the accumulation of CT-truncat
41 sociated with cavitation, necrosis and acute axonal pathology (spheroids), in both grey and white mat
42 gro-striatal axonal terminals leads to early axonal pathology, synaptic disruption, dysfunction of do
46 oduced a concentration-dependent increase in axonal pathology within the striatum reflected by the am
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