| 11. |
- Haglund, Mattias, et al.
(författare)
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Severe Cerebral Amyloid Angiopathy Characterizes an Underestimated Variant of Vascular Dementia.
- 2004
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Ingår i: Dementia and Geriatric Cognitive Disorders. - : S. Karger AG. - 1420-8008 .- 1421-9824. ; 18:2, s. 132-137
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Tidskriftsartikel (refereegranskat)abstract
- Cerebral amyloid angiopathy (CAA) is a frequent finding on neuropathological examination of patients with Alzheimer’s disease (AD). A recent study from our laboratory showed that CAA also frequently occurred in vascular dementia with additional mild Alzheimer encephalopathy (VaD-ae, i.e. Alzheimer pathology that does not fulfill criteria for AD). Because CAA is associated with cerebral hemorrhages and infarctions, it is of significant interest to confirm or dismiss the hypothesis that CAA contributes clinically in the many patients that present with VaD-ae. Therefore, we examined entire temporal lobes of 11 VaD-ae cases and 11 age-matched AD cases with Aβ immunohistochemistry. Six of 11 VaD-ae cases had severe CAA, more extensive than in any AD case. There was a trend toward more cortical infarctions in this group, indicating that CAA in VaD may be of clinical importance and an underestimated cause of dementia.
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| 12. |
- Larsson, Elna-Marie, et al.
(författare)
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Magnetic resonance imaging and histopathology in dementia, clinically of frontotemporal type
- 2000
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Ingår i: Dementia and Geriatric Cognitive Disorders. - : S. Karger AG. - 1420-8008 .- 1421-9824. ; 11:3, s. 123-134
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Tidskriftsartikel (refereegranskat)abstract
- The magnetic resonance imaging (MRI) and computed tomography findings in 28 patients with the clinical diagnosis of frontotemporal dementia (FTD) were compared with the findings in a control group of 76 individuals without dementia or stroke. A pattern of frontal and temporal atrophy with predominantly frontal white matter changes was found in the FTD patients, and this was significantly different from the radiological findings in the control group. Six of the FTD patients have undergone autopsy. Histopathological evaluation showed a primary cortical degenerative disease (frontal lobe degeneration of non-Alzheimer type) in 3 of them, and primary white matter disorder, mainly frontal, of basically ischemic type (selective incomplete white matter infarction) in 3 of them. MRI could be a helpful tool to support the clinical diagnosis FTD, especially in young patients. MRI may also be helpful for the differentiation of a primary neurodegenerative from a mainly ischemic-vascular type of dementia.
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| 13. |
- Larsson, Elna-Marie, et al.
(författare)
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MRI with diffusion tensor imaging post-mortem at 3.0 T in a patient with frontotemporal dementia.
- 2004
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Ingår i: Dementia and Geriatric Cognitive Disorders. - : S. Karger AG. - 1420-8008 .- 1421-9824. ; 17:4, s. 316-319
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Tidskriftsartikel (refereegranskat)abstract
- The formalin-fixed brain of a patient with clinically diagnosed frontotemporal dementia (FTD) was examined post-mortem using magnetic resonance imaging (MRI) with diffusion tensor imaging (DTI) at 3.0 T. Frontotemporal atrophy as well as bilateral frontal white matter abnormalities were seen. The white matter changes were slightly more extensive on DTI than on conventional MRI. Correlation with histopathology of the corresponding regions revealed typical frontal lobe degeneration of non-Alzheimer type, with mild frontotemporal degeneration in the outer cortical layers and a moderate frontal white matter gliosis with demyelination. Post-mortem MRI/DTI with histopathologic correlation will enhance our understanding of the basis of white matter changes observed in dementia patients and may improve the in vivo MRI/DTI diagnostic assessment in FTD.
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| 14. |
- Leys, Didier, et al.
(författare)
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Vascular Dementia
- 2003
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Ingår i: Evidence based Dementia Practice. - : Wiley. - 9780470752340 - 0632052961 - 9780632052967 ; , s. 260-287
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Bokkapitel (refereegranskat)
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| 15. |
- Risberg, Jarl, et al.
(författare)
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Posterior cingulate cortex in familiar Alzheimer’s disease: A clinicopathological and brain imaging study
- 2003
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Ingår i: Journal of the International Neuropsychological Society. - 1355-6177. ; 9, s. 174-174
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Konferensbidrag (refereegranskat)abstract
- The degenerative process in Alzheimer´s disease (AD) follows a temporal and topographic pattern of early and accentuated involvement of temporal limbic, parietal and posterior cingulate cortices. We have studied a pedigree with four generations suffering from early onset AD linked to a presenilin-1 gene mutation. This family now contains 7 AD cases, neuropathologically confirmed in four cases of three generations. In all four cases the degeneration was most pronounced in the temporoparietal cortex, but also engaged central grey structures such as the claustrum, central thalamic and brain stem nuclei. There was a consistent and severe degeneration in posterior cingulate cortex in contrast to a compara¬tively spared anterior cingulum. Regional cerebral blood flow (rCBF) was studied repeated¬ly with 133-xenon inhalation and SPECT methods. The rCBF measurements showed the typical cortical pathology of AD with bilateral decreases in temporoparietal and posterior cingulate cortices, accentuating over time and spreading anteriorly. There was a very good correspondence between clinical, neuroimaging and neuropathological features. Our findings indicate that posterior cingulum is a major locus for functional and structural vulnerability in both familial and sporadic forms of AD, something that might be used for diagnostic purposes together with possible posterior cingulate symptomatology.
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| 16. |
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| 17. |
- Sjogren, M, et al.
(författare)
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Negative neurofilament light and tau immunostaining in frontotemporal dementia
- 2004
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Ingår i: Frontotemporal Dementias 4th International Conference (Dementia and Geriatric Cognitive Disorders). - : S. Karger AG. - 1421-9824 .- 1420-8008. ; 17:4, s. 346-349
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Konferensbidrag (refereegranskat)abstract
- We investigated the immunohistochemical stainability of phosphorylated tau and the light (NFL), intermediate (NFM), and heavy (NFH) neurofilament proteins in postmortem brain tissue from 8 patients with frontotemporal dementia (FTD), for comparison with 6 patients with Alzheimer's disease (AD), and 6 normal controls. In the FTD group, the neuropathological diagnosis was pure frontal-lobe degeneration of non-Alzheimer type (FLD) in 6 cases and in the remaining 2 cases mixed FLD-AD and frontal AD, respectively. The staining for tau was negative in 5 of the FLD cases and faintly positive in 1, but positive in all AD cases. The antibodies against NFM and NFH stained positive in FLD, AD, and controls, whereas the staining for NFL was negative in all FLD cases and positive in 1 AD case and in the controls. These findings regarding NFL and tau staining may be useful in the differential diagnosis of FLD and AD. Copyright (C) 2004 S. Karger AG, Basel.
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| 18. |
- Sjöbeck, Martin, et al.
(författare)
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Alzheimer's disease and the cerebellum: a morphologic study on neuronal and glial changes
- 2001
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Ingår i: Dementia and Geriatric Cognitive Disorders. - : S. Karger AG. - 1420-8008 .- 1421-9824. ; 12:3, s. 211-218
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Tidskriftsartikel (refereegranskat)abstract
- Structural manifestations of Alzheimer's disease (AD) including neuronal loss were investigated in 12 cases of AD and in 10 healthy age-matched controls, with focus on the cerebellum. Linear Purkinje cell (PC) density was measured in the vermis and cerebellar hemispheres. Neurons were also counted in the inferior olivary nucleus. In vermis of the AD cases, the mean PC number was significantly lower (p = 0.019) than in the controls. The neurons in the inferior olive were similarly fewer, though not significantly (p = 0.13). Molecular layer gliosis and atrophy in the vermis was clearly severer in AD than in the controls. Features typical of cerebral Alzheimer encephalopathy (plaques, tangles and microvacuolization) were inconspicious. The structural cerebellar changes in the AD cases were thus neuronal loss, atrophy and gliosis, judged to represent the disease process, and with a main involvement in the vermis. This may be reflected in some of the symptoms and signs seen in AD, signs that are generally overlooked or judged to be of noncerebellar origin.
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| 19. |
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| 20. |
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