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176 results on '"Rossor, M.N."'

51. Early cognitive decline in Creutzfeldt-Jakob disease occurring in recipients of pituitary-derived human growth hormone. (Proceedings)

Author

Cordery, R.J., Hall, M., Cipolotti, L., Davidson, L., Adlard, P., and Rossor, M.N.

Subjects
Dementia -- Development and progression -- Care and treatment, Pituitary hormones -- Health aspects, Creutzfeldt-Jakob disease -- Care and treatment -- Development and progression, Health, Psychology and mental health, Care and treatment, Development and progression, Health aspects
Abstract

Most cases of Creutzfeldt-Jakob disease (CJD] in recipients of human cadaveric growth hormone, present with a cerebellar syndrome. Dementia is thought to occur late and as a minor feature of [...]

Published
2002

52. Corticobasal degeneration and progressive supranuclear palsy share a common tau haplotype

Author

Houlden, H., primary, Baker, M., additional, Morris, H.R., additional, MacDonald, N., additional, Pickering-Brown, S., additional, Adamson, J., additional, Lees, A.J., additional, Rossor, M.N., additional, Quinn, N.P., additional, Kertesz, A., additional, Khan, M.N., additional, Hardy, J., additional, Lantos, P.L., additional, St. George-Hyslop, P., additional, Munoz, D.G., additional, Mann, D., additional, Lang, A.E., additional, Bergeron, C., additional, Bigio, E.H., additional, Litvan, I., additional, Bhatia, K.P., additional, Dickson, D., additional, Wood, N.W., additional, and Hutton, M., additional

Published
2001
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54. Progressive cerebral atrophy in MS

Author

Fox, N.C., primary, Jenkins, R., additional, Leary, S.M., additional, Stevenson, V.L., additional, Losseff, N.A., additional, Crum, W.R., additional, Harvey, R.J., additional, Rossor, M.N., additional, Miller, D.H., additional, and Thompson, A.J., additional

Published
2000
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58. Evidence for allelic heterogeneity in familial early-onset Alzheimer's disease

Author

Duijn, C.M. (Cornelia) van, Hardy, J. (John), Goate, A.M. (Alison), Rossor, M.N. (Martin), Vandenberghe, A. (Anton), Martin, J-J. (Jean-Jacques), Mullan, M.J., Broeckhoven, C. (Christine) van, Hofman, A. (Albert), Duijn, C.M. (Cornelia) van, Hardy, J. (John), Goate, A.M. (Alison), Rossor, M.N. (Martin), Vandenberghe, A. (Anton), Martin, J-J. (Jean-Jacques), Mullan, M.J., Broeckhoven, C. (Christine) van, and Hofman, A. (Albert)

Abstract

Age of onset was examined for 139 members of 30 families affected by early-onset AD. Most (77%) of the variance of age of onset derived from differences between rather than within families. The constancy of age of onset within families was also observed in an analysis restricted to families derived from a population-based epidemiological study with complete ascertainment of early-onset AD. Furthermore, we observed clustering of age of onset within those families that support linkage to the predisposing locus on chromosome 21. Our data are compatible with the view that allelic heterogeneity at the AD locus may account for the similarity in age of onset within families. This finding may be of value for scientific studies of AD as well as for genetic counselling.

Published
1991

75. The prevalence of oligoclonal bands in the CSF of patients with primary neurodegenerative dementia.

Author

Janssen, J.C., Godbolt, A.K., Ioannidis, P., Thompson, E.J., and Rossor, M.N.

Subjects
DEMENTIA, DEGENERATION (Pathology), CEREBROSPINAL fluid, IMMUNE response, NEUROBEHAVIORAL disorders, PSYCHOSES
Abstract

Background:. Recent guidelines from the United States and Europe on the diagnosis and management of dementia include advice that younger patients with dementia should undergo CSF examination, which frequently includes analysis for oligoclonal bands (OCB). The presence of CNS specific OCB has traditionally been considered suggestive of an inflammatory aetiology, although the interpretation of such a finding in the presence of a normal CSF white cell count and protein is more difficult. Methods:. We reviewed retrospectively the prevalence of OCB, determined using agarose isoelectric focusing, in a series of 131 well characterised patients with a final diagnosis of a degenerative dementia who had undergone CSF examination. Results:. The mean age of the patients was 60.0 (SD 8.4) years. Seventy (53%) patients had Alzheimer’s disease (AD), forty seven (36 %) had frontotemporal lobar degeneration (FTLD), seven (5%) had Dementia with Lewy bodies and the remaining seven (5%) patients had other rarer neurodegenerative dementias. Neuropathological examination had been performed in fifteen (11%) patients. CNS specific OCB were present in nine (7%) patients in this cohort, all of whom had normal CSF white cell counts: four AD patients (a prevalence of 6%), four FTLD patients (a prevalence of 9%), and one patient with Creutzfeldt-Jakob disease (a prevalence of 25%). Investigation of these patients, including two with neuropathologically verified AD and one with post-mortem confirmed CJD, did not reveal an alternative aetiology for their dementia. Conclusion:. A central immune response can occur in primary neurodegenerative dementias, albeit uncommonly. [ABSTRACT FROM AUTHOR]

Published
2004
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76. Neurochemical characteristics of early and late onset types of Alzheimer's disease.

Author

Rossor, M.N., Iversen, L.L., Reynolds, G.P., Mountjoy, C.Q., and Roth, M.

Subjects
*ALZHEIMER'S disease research, *PATIENTS, *DISEASES
Abstract

Examines the neurochemical characteristics of Alzheimer's diseases. Causes of Alzheimer's disease; Differences in the patterns of neurochemical abnormality between young and old patients; Suggestions that the disease may reflect an acceleration of the aging process.

Published
1984
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77. Progressive frontal gait disturbance with atypical Alzheimer's disease and corticobasal degeneration

Author

Rossor, M.N., Tyrrell, P.J., Warrington, E.K., Marsden, C.D., Thompson, P.D., and Lantos, P.

Abstract

ObjectivesThe clinical neuropsychological, neuroradiological, and neuropathological description of two patients presenting with a frontal gait disturbance. MethodsClinical case note review, neuropsychological assessment, functional imaging with 15O 2 and 18F-fluorodopa PET, and neuropathology. ResultsBoth patients presented with frontal gait impairment and only later developed more widespread cognitive impairment. In both cases 15O 2 PET disclosed focal hypometabolism in the medial frontal lobes and in one patient 18F-fluorodopa uptake into the caudate and putamen was normal. The neuropathological examination in one patient showed Alzheimer's histopathology together with large swollen eosinophilic neurons characteristic of corticobasal degeneration, which were particularly prominent in the medial frontal lobes. ConclusionFocal degeneration of the medial frontal lobes may present as an isolated gait disturbance and should be considered in the differential diagnosis of patients who present without an obvious structural abnormality on neuroimaging.

Published
1999

78. Psychiatric symptoms in patients with focal cortical degeneration

Author

Lawrence, R.M., Ronca, M.A., Tyrrell, P., and Rossor, M.N.

Abstract

The psychiatric phenomenology exhibited by a mixed group of patients with focal cortical degeneration (FCD) is described. The diagnosis of FCD was made in the presence of a slowly progressive focal neuropsychological deficit without evidence of infarct or neoplasm. Localized or asymmetric atrophy was present on neuroimaging (CT or MRI) and positron emission tomography demonstrated focal hypometabolism or in those assessed later in the disease an area of maximal hypometabolism which correlated with the neuropsychological deficit. FCD patients exhibited prominent obsessive–compulsive behaviour. Obsessive–compulsive features were often repetitive, stereotyped and bizarre and occurred in association with frontal and left temporal atrophy and hypometabolism and were absent in those with predominant posterior cortical pathology.

Published
1994
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79. Familial dementia lacking specific pathological features presenting with clinical features of corticobasal degeneration

Author

Brown, J., Rossor, M.N., and Lantos, P.L.

Abstract

A family is described in which one member presented with symptoms and signs suggestive of corticobasal degeneration and a sibling presented with features of a frontal lobe dementia. Their mother developed a presenile dementia and movement disorder. At postmortem examination the member with clinical corticobasal degeneration had non-specific pathological features. Therefore, the clinical features of corticobasal degeneration can occur with non-specific pathological changes. Within a pedigree, different members can present with different clinical syndromes, which may reflect variation in the distribution and severity of the pathological process.

Published
1998

81. Chromosome 14 familial Alzheimer's disease: the clinical and neuropathological characteristics of a family with a leucine→serine (L250S) substitution at codon 250 of the presenilin 1 gene

Author

Harvey, R.J., Roques, P.K., Fox, N.C., Rossor, M.N., Ellison, D., Hardy, J., Hutton, M., and Collinge, J.

Abstract

Background Seven affected members are described from a kindred with autosomal dominant familial Alzheimer's disease associated with a novel mutation in the presenilin 1 (PS1) gene on chromosome 14 that results in a leucine to serine substitution at codon 250 (L250S). Method Clinical information on the pedigree was collected directly from family members including affected members and their carers and also from hospital records. Results Detailed clinical information was available on five members. All had an early age at onset with a median age of 52 (95% confidence interval (95% CI) 49.4-54.9). Age at onset varied between 49 and 56 years, with duration of illness varying between six years and 15 years. Myoclonus, depression, and psychosis were features of this pedigree; seizures were not reported. Conclusions PS1 L250S familial Alzheimer's disease is an early onset form of Alzheimer's disease with clinical features similar to other reported familial Alzheimer's disease pedigrees, except that seizures were absent.

Published
1998

82. Parkinson's disease and Alzheimer's disease as disorders of the isodendritic core.

Author

Rossor, M.N.

Subjects
*PARKINSON'S disease, *ALZHEIMER'S disease
Abstract

Focuses on the characterization of Parkinson's disease and Alzheimer's disease as disorders of the isodentritic core. Consequence of the loss of ascending projections from the isodendritic cells; Enhancement of the transmitter release by neurones or by direct agonists; Creation of an opportunity for neurotransmitter replacement treatment.

Published
1981
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83. EEG abnormalities in frontotemporal lobar degeneration

Author

Chan, D., Walters, R.J., Sampson, E.L., Schott, J.M., Smith, S.J., and Rossor, M.N.

Abstract

The EEG appearances in patients with frontotemporal lobar degeneration (FTLD) were compared with those in patients with Alzheimer disease (AD). EEG abnormalities were found in 61 of FTLD patients, with the degree of EEG abnormality increasing with dementia severity. There was no significant difference in the severity of EEG abnormality between the FTLD and AD patient groups. These data suggest a need for reappraisal of the role of the EEG in the diagnostic differentiation of FTLD from AD.

Published
2004

84. Sequence analysis of tau in familial and sporadic progressive supranuclear palsy

Author

Wood, N.W., Morris, H.R., Lees, A.J., Katzenschlager, R., Janssen, J.C., Brown, J.M., Ozansoy, M., Quinn, N., Revesz, T., Rossor, M.N., and Daniel, S.E.

Abstract

Progressive supranuclear palsy (PSP) is a tau deposition neurodegenerative disorder which usually occurs in sporadic form and is associated with a common variant of the tau gene. Rare familial forms of PSP have been described. Recently familial frontotemporal dementia linked to chromosome 17 (FTDP-17) has been shown to be due to mutations in tau and there may be a clinical and pathological overlap between PSP and FTDP-17. In this study we have analysed the tau sequence in two small families with PSP, and a number of clinically typical and atypical sporadic cases with pathological confirmation of the diagnosis. The tau mutations described in FTDP-17 were not found in the most clinically diagnosed patients with PSP. This suggests that usually FTDP-17 and PSP, including the rare familial form of PSP, are likely to be separate conditions and that usually PSP and typical PSP-like syndromes are not due to mutations in tau.

Published
2002

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