Novel eosinophilic neuronal cytoplasmic inclusions in the external cuneate nucleus of humans

2016 ◽  
Vol 36 (5) ◽  
pp. 441-447 ◽  
Author(s):  
Masako Ito ◽  
Keiko Nakamura ◽  
Fumiaki Mori ◽  
Yasuo Miki ◽  
Kunikazu Tanji ◽  
...  
Keyword(s):  
Cuneate Nucleus ◽  
Cytoplasmic Inclusions ◽  
External Cuneate Nucleus ◽  
Neuronal Cytoplasmic Inclusions

Somatotopic organization of the external cuneate nucleus in albino rats

1974 ◽  
Vol 77 (1) ◽  
pp. 1-23 ◽  
Author(s):  
Suzann K. Campbell ◽  
T.D. Parker ◽  
Wally Welker
Keyword(s):  
Albino Rats ◽  
Cuneate Nucleus ◽  
Somatotopic Organization ◽  
External Cuneate Nucleus

Maturation process of TDP-43-positive neuronal cytoplasmic inclusions in amyotrophic lateral sclerosis with and without dementia

2008 ◽  
Vol 116 (2) ◽  
pp. 193-203 ◽  
Author(s):  
Fumiaki Mori ◽  
Kunikazu Tanji ◽  
Hai-Xin Zhang ◽  
Yasushi Nishihira ◽  
Chun-Feng Tan ◽  
...  
Keyword(s):  
Amyotrophic Lateral Sclerosis ◽  
Maturation Process ◽  
Cytoplasmic Inclusions ◽  
Neuronal Cytoplasmic Inclusions ◽  
Lateral Sclerosis

scholarly journals Hippocampal α-synuclein pathology correlates with memory impairment in multiple system atrophy

Brain ◽  
2020 ◽  
Vol 143 (6) ◽  
pp. 1798-1810 ◽  
Author(s):  
Yasuo Miki ◽  
Sandrine C Foti ◽  
Daniela Hansen ◽  
Kate M Strand ◽  
Yasmine T Asi ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Multiple System Atrophy ◽  
Dentate Gyrus ◽  
Memory Impairment ◽  
Cytoplasmic Inclusions ◽  
Glial Cytoplasmic Inclusions ◽  
Cornu Ammonis ◽  
Neuronal Cytoplasmic Inclusions ◽  
With Memory ◽  
Normal Cognition

Abstract Recent post-mortem studies reported 22–37% of patients with multiple system atrophy can develop cognitive impairment. With the aim of identifying associations between cognitive impairment including memory impairment and α-synuclein pathology, 148 consecutive patients with pathologically proven multiple system atrophy were reviewed. Among them, 118 (79.7%) were reported to have had normal cognition in life, whereas the remaining 30 (20.3%) developed cognitive impairment. Twelve of them had pure frontal-subcortical dysfunction, defined as the presence of executive dysfunction, impaired processing speed, personality change, disinhibition or stereotypy; six had pure memory impairment; and 12 had both types of impairment. Semi-quantitative analysis of neuronal cytoplasmic inclusions in the hippocampus and parahippocampus revealed a disease duration-related increase in neuronal cytoplasmic inclusions in the dentate gyrus and cornu ammonis regions 1 and 2 of patients with normal cognition. In contrast, such a correlation with disease duration was not found in patients with cognitive impairment. Compared to the patients with normal cognition, patients with memory impairment (pure memory impairment: n = 6; memory impairment + frontal-subcortical dysfunction: n = 12) had more neuronal cytoplasmic inclusions in the dentate gyrus, cornu ammonis regions 1–4 and entorhinal cortex. In the multiple system atrophy mixed pathological subgroup, which equally affects the striatonigral and olivopontocerebellar systems, patients with the same combination of memory impairment developed more neuronal inclusions in the dentate gyrus, cornu ammonis regions 1, 2 and 4, and the subiculum compared to patients with normal cognition. Using patients with normal cognition (n = 18), frontal-subcortical dysfunction (n = 12) and memory impairment + frontal-subcortical dysfunction (n = 18), we further investigated whether neuronal or glial cytoplasmic inclusions in the prefrontal, temporal and cingulate cortices or the underlying white matter might affect cognitive impairment in patients with multiple system atrophy. We also examined topographic correlates of frontal-subcortical dysfunction with other clinical symptoms. Although no differences in neuronal or glial cytoplasmic inclusions were identified between the groups in the regions examined, frontal release signs were found more commonly when patients developed frontal-subcortical dysfunction, indicating the involvement of the frontal–subcortical circuit in the pathogenesis of frontal-subcortical dysfunction. Here, investigating cognitive impairment in the largest number of pathologically proven multiple system atrophy cases described to date, we provide evidence that neuronal cytoplasmic inclusion burden in the hippocampus and parahippocampus is associated with the occurrence of memory impairment in multiple system atrophy. Further investigation is necessary to identify the underlying pathological basis of frontal-subcortical dysfunction in multiple system atrophy.

Vestibulospinal effects on neurons in different regions of the gray matter of the cat upper cervical cord

1996 ◽  
Vol 76 (4) ◽  
pp. 2439-2446 ◽  
Author(s):  
N. Isu ◽  
D. B. Thomson ◽  
V. J. Wilson
Keyword(s):  
Gray Matter ◽  
Vestibular Nuclei ◽  
Afferent Input ◽  
Ventral Horn ◽  
Cervical Cord ◽  
Cuneate Nucleus ◽  
External Cuneate Nucleus ◽  
Upper Cervical ◽  
Neck Motoneurons ◽  
Stimulation Of

1. Previous studies of vestibular effects on the upper cervical cord have concentrated on the lateral and medial vestibulospinal tracts and on the actions that they exert on neck motoneurons and other neurons in the ventral horn. It is known, however, that both the rostral and the caudal areas of the vestibular nuclei (VN) give rise to axons that are located in the dorsal and dorsolateral funiculi and that terminate in the dorsal horn. A primary goal of our experiments was to investigate the effect of VN stimulation on neurons dorsal to lamina VII. 2. In decerebrate cats with the caudal cerebellar vermis removed, we stimulated different areas of the VN with an array of electrode. The area of stimulation extended from the caudal tip of the descending nucleus to Deiters' nucleus, and was divided into rostral and caudal halves with the use of the descending nucleus as a reference. For control purposes some stimulating points were placed in the external cuneate nucleus and restiform body. 3. We tested the effects of VN stimulation on spontaneously firing neurons in the ipsilateral C2 and C3 segments. For purposes of classification the gray matter was divided into four zones corresponding approximately to laminae 1-IV, V-VI, VII, and VIII of Rexed. Overall, the activity of 39 of 84 neurons was influenced from one or more stimulating sites. For six cells there was some possibility of current spread to the external cuneate nucleus or to the underlying reticular formation. 4. VN-evoked effects could consist of facilitation, or, less often, inhibition. In the majority of facilitated neurons conditioning stimuli evoked a synchronized, short-latency, increase in firing probability. When evoked by single stimuli this facilitation was considered monosynaptic. Facilitation that was diffuse, or that was only evoked by two or more stimuli, presumably involved more complex pathways. The latency of inhibition could not be measured, but was short. 5. Stimulation of either the rostral or caudal VN had no effect on neurons in laminae I-IV. Electrodes placed rostrally had little effect on neurons in laminae V-VI, but influenced more than half the neurons in laminae VII-VIII. Conversely, electrodes placed caudally were most effective on cells in laminae V-VII, although they also influenced some neurons in lamina VIII. 6. Stimulation of the dorsal rami influenced most neurons in laminae V-VI, and about a quarter of the neurons in laminae VII-VIII. When tested, there was often convergence between vestibulospinal and peripheral inputs. 7. Our results provide physiological evidence that vestibulospinal fibers influence neurons not only in laminae VII and VIII, but also as far dorsally as lamina V. Fibers that influence neurons in laminae V and VI originate primarily in the caudal areas of the VN. As suggested previously on anatomic grounds, the projection to the dorsal laminae, which is predominantly facilitatory, often converges with afferent input and can therefore modulate its influence on spinal neurons.

scholarly journals Clinicopathological Studies of Some Non-Alzheimer Dementing Diseases

1986 ◽  
Vol 13 (S4) ◽  
pp. 483-489 ◽  
Author(s):  
David Munoz-Garcia ◽  
Samuel K. Ludwin
Keyword(s):  
Morphological Changes ◽  
Cerebral Atrophy ◽  
Paired Helical Filaments ◽  
Pick's Disease ◽  
Neuronal Dysfunction ◽  
Pick’S Disease ◽  
Cytoplasmic Localization ◽  
Adult Onset ◽  
Cytoplasmic Inclusions ◽  
Neuronal Cytoplasmic Inclusions

Abstract:The brains of most demented patients show at autopsy the lesions of Alzheimer's disease (AD). However, the brains of other demented patients show either no morphological changes or lesions distinct from those of AD. We report clinicopathological studies on two diseases in this latter group. The study of these diseases can improve our understanding of AD.Pick's disease is characterized by dementia, lobar cerebral atrophy, and neuronal cytoplasmic inclusions. Most cases, which we have called “classical”, show inclusions made up of straight fibrils that are immunologically cross-reactive with the paired helical filaments of AD. In other “generalized” cases, similar fibrils are coated by granular material and are less reactive with anticytoskeletal antibodies.In contrast to the cytoplasmic localization of the lesions in Pick's disease, it is the cell nucleus that shows abnormalities in neuronal intranuclear hyaline inclusion disease. This disease can present clinically as dementia of adult onset. Thus, either nuclear or cytoplasmic lesions can produce a pattern of neuronal dysfunction resulting in dementia.

Patterns of degeneration in the external cuneate nucleus after multiple dorsal rhizotomies

1977 ◽  
Vol 175 (2) ◽  
pp. 181-205 ◽  
Author(s):  
Jeffrey M. Rosenstein ◽  
Robert B. Page ◽  
Alphonse E. Leure-DuPree
Keyword(s):  
Cuneate Nucleus ◽  
External Cuneate Nucleus

XIAP immunoreactivity in glial and neuronal cytoplasmic inclusions in multiple system atrophy

2014 ◽  
Vol 33 (01) ◽  
pp. 76-83 ◽  
Author(s):  
Yasuhiro Kawamoto ◽  
Hidefumi Ito ◽  
Masafumi Ihara ◽  
Ryosuke Takahashi
Keyword(s):  
Multiple System Atrophy ◽  
Cytoplasmic Inclusions ◽  
Neuronal Cytoplasmic Inclusions
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