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  • 1
    Electronic Resource
    Electronic Resource
    Immunoreactivity profile of hippocampal CA2/3 neurites in diffuse Lewy body disease (1994)
    Springer
    Acta neuropathologica 87 (1994), S. 269-276 
    Details
    ISSN: 1432-0533
    Keywords: Diffuse Lewy Body Disease ; Hippocampus ; Neurites ; Neurofilament ; Ubiquitin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Ubiquitin-immunoreactive dystrophic neurites in the CA2/3 region of the hippocampus are characteristic of diffuse Lewy body disease (DLBD). The origin of dystrophic CA2/3 neurites is unknown, but their extent correlates with the number of cortical Lewy bodies (LBs). To examine the molecular composition of these lesions, hippocampal sections were obtained at postmortem from cases of DLBD, Parkinson's disease and Alzheimer's disease. The tissue samples were fixed in a variety of fixatives and immunostained with antibodies to ubiquitin, ubiquitin C-terminal hydrolase (PGP9.5), neurofilament protein subunits, tau protein, paired helical filaments and tyrosine hydroxylase (TH). In addition to being ubiquitin positive, both cortical LBs and CA2/3 dystrophic neurites were positive with a neurofilament monoclonal antibody (RM032) and PGP9.5; however, fewer lesions were detected with these antibodies compared to ubiquitin immunocyto-chemistry. The dystrophic CA2/3 neurites were not stained with antibodies to tau proteins, paired helical filaments or TH. Absence of TH immunoreactivity suggests that CA2/3 neuritic processes are not derived from brain stem dopaminergic afferents to the hippocampus. Since CA2/3 neurites are immunologically similar to cortical LB, the pathogenesis of these lesions may be similar. Characterization of dystrophic CA2/3 neurites and cortical LBs may clarify how these lesions contribute to the emergence of dementia in DLBD.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00296742
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    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Immunoreactivity profile of hippocampal CA2/3 neurites in diffuse Lewy body disease (1994)
    Springer
    Acta neuropathologica 87 (1994), S. 269-276 
    Details
    ISSN: 1432-0533
    Keywords: Key words: Diffuse Lewy Body Disease – Hippocampus – Neurites – Neurofilament – Ubiquitin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Ubiquitin-immunoreactive dystrophic neurites in the CA2/3 region of the hippocampus are characteristic of diffuse Lewy body disease (DLBD). The origin of dystrophic CA2/3 neurites is unknown, but their extent correlates with the number of cortical Lewy bodies (LBs). To examine the molecular composition of these lesions, hippocampal sections were obtained at postmortem from cases of DLBD, Parkinson's disease and Alzheimer's disease. The tissue samples were fixed in a variety of fixatives and immunostained with antibodies to ubiquitin, ubiquitin C-terminal hydrolase (PGP9.5), neurofilament protein subunits, tau protein, paired helical filaments and tyrosine hydroxylase (TH). In addition to being ubiquitin positive, both cortical LBs and CA2/3 dystrophic neurites were positive with a neurofilament monoclonal antibody (RM032) and PGP9.5; however, fewer lesions were detected with these antibodies compared to ubiquitin immunocytochemistry. The dystrophic CA2/3 neurites were not stained with antibodies to tau proteins, paired helical filaments or TH. Absence of TH immunoreactivity suggests that CA2/3 neuritic processes are not derived from brain stem dopaminergic afferents to the hippocampus. Since CA2/3 neurites are immunologically similar to cortical LB, the pathogenesis of these lesions may be similar. Characterization of dystrophic CA2/3 neurites and cortical LBs may clarify how these lesions contribute to the emergence of dementia in DLBD.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00296742
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    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Association of apolipoprotein ɛ4 allele and neuropathologic findings in patients with dementia (1995)
    Springer
    Acta neuropathologica 90 (1995), S. 239-243 
    Details
    ISSN: 1432-0533
    Keywords: Apolipoprotein E ; Dementia ; Diffuse Lewy body disease ; Alzheimer's disease ; Parkinson's disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Apolipoprotein E (APOE) is a lipoprotein expressed in liver and brain as one of three isoforms (APOE 2, APOE 3 and APOE 4). Recent findings suggest that the presence of APOE 4 is associated with an increased risk for both familial Alzheimer's disease and late-onset Alzheimer's disease. We extended these observations by determining the frequency of APOE alleles in patients with pathologically confirmed Alzheimer's Disease (AD), Parkinson's disease (PD), diffuse Lewy Body disease (DLBD), AD with concomitant PD pathology, demented PD patients without or with concomitant AD pathology and in schizophrenics with a progressive dementia (SCHIZ+DEM). The APOE genotype was determined by restriction digestion of polymerase chain reaction-amplified DNA isolated from frozen brain samples. The frequency of the APOE ɛ4 allele was highest among sporadic AD and DLBD patients (0.30 and 0.38, respectively) and lowest in the SCHIZ+DEM and non-demented PD patients (0.06 and 0.1, respectively). Thus, the APOE ɛ4 allele is over-represented selectively in patients with dementias associated with plaques and tangles and/or cortical Lewy bodies, but not in demented schizophrenics or non-demented PD patients.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00296506
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    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Association of apolipoprotein ε4 allele and neuropathologic findings in patients with dementia (1995)
    Springer
    Acta neuropathologica 90 (1995), S. 239-243 
    Details
    ISSN: 1432-0533
    Keywords: Key words Apolipoprotein E ; Dementia ; Diffuse Lewy body disease ; Alzheimer's disease ; Parkinson's disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Apolipoprotein E (APOE) is a lipoprotein expressed in liver and brain as one of three isoforms (APOE 2, APOE 3 and APOE 4). Recent findings suggest that the presence of APOE 4 is associated with an increased risk for both familial Alzheimer's disease and late-onset Alzheimer's disease. We extended these observations by determining the frequency of APOE alleles in patients with pathologically confirmed Alzheimer's Disease (AD), Parkinson's disease (PD), diffuse Lewy Body disease (DLBD), AD with concomitant PD pathology, demented PD patients without or with concomitant AD pathology and in schizophrenics with a progressive dementia (SCHIZ+DEM). The APOE genotype was determined by restriction digestion of polymerase chain reaction-amplified DNA isolated from frozen brain samples. The frequency of the APOE ε4 allele was highest among sporadic AD and DLBD patients (0.30 and 0.38, respectively) and lowest in the SCHIZ+DEM and non-demented PD patients (0.06 and 0.1, respectively). Thus, the APOE ε4 allele is over-represented selectively in patients with dementias associated with plaques and tangles and/or cortical Lewy bodies, but not in demented schizophrenics or non-demented PD patients.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00296506
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    Paper (German National Licenses)
    Fulltext
  • 5
    Electronic Resource
    Electronic Resource
    Paired helical filament tau (PHFtau) in Niemann-Pick type C disease is similar to PHFtau in Alzheimer's disease (1995)
    Springer
    Acta neuropathologica 90 (1995), S. 547-551 
    Details
    ISSN: 1432-0533
    Keywords: Cholesterol metabolism ; Cytoskeleton ; Dementia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Niemann-Pick Type C disease (NPC) is a cholesterol storage disease with defects in the intracellular trafficking of exogenous cholesterol derived from low density lipoproteins. In NPC cases with a chronic progressive course, neurofibrillary tangles (NFTs) that consist of paired helical filaments (PHFs) have been reported. To determine if NPC tangles contain abnormal tau proteins (known as PHFtau) similar to those found in Alzheimer's disease (AD) tangles, we examined the brains of five NPC cases by immunohistochemical and Western blot methods using a library of antibodies to defined epitopes of PHFtau. We show here that PHFtau in tangle-rich NPC brains is indistinguishable from PHFtau in AD brains. We speculate, that the generation of PHFtau in NPC may induce a cascade of pathological events that contribute to the widespread degeneration of neurons, and that these events may be similar in NPC and AD.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00318566
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    Paper (German National Licenses)
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  • 6
    Electronic Resource
    Electronic Resource
    Paired helical filament tau (PHFtau) in Niemann-Pick type C disease is similar to PHFtau in Alzheimer's disease (1995)
    Springer
    Acta neuropathologica 90 (1995), S. 547-551 
    Details
    ISSN: 1432-0533
    Keywords: Key words Cholesterol metabolism ; Cytoskeleton ; Dementia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Niemann-Pick Type C disease (NPC) is a cholesterol storage disease with defects in the intracellular trafficking of exogenous cholesterol derived from low density lipoproteins. In NPC cases with a chronic progressive course, neurofibrillary tangles (NFTs) that consist of paired helical filaments (PHFs) have been reported. To determine if NPC tangles contain abnormal tau proteins (known as PHFtau) similar to those found in Alzheimer's disease (AD) tangles, we examined the brains of five NPC cases by immunohistochemical and Western blot methods using a library of antibodies to defined epitopes of PHFtau. We show here that PHFtau in tangle-rich NPC brains is indistinguishable from PHFtau in AD brains. We speculate, that the generation of PHFtau in NPC may induce a cascade of pathological events that contribute to the widespread degeneration of neurons, and that these events may be similar in NPC and AD.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00318566
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 7
    Electronic Resource
    Electronic Resource
    Convergence of Lewy bodies and neurofibrillary tangles in amygdala neurons of Alzheimer’s disease and Lewy body disorders (1996)
    Springer
    Acta neuropathologica 91 (1996), S. 475-481 
    Details
    ISSN: 1432-0533
    Keywords: Key words Amygdala ; Lewy bodies ; Neurofibrillary ; tangles ; Parkinson’s disease ; Dementia pathology
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Amygdalae of patients with Alzheimer’s disease (AD), Parkinson’s disease, Down’s syndrome, diffuse Lewy body disease or a combination of these diseases were probed with antibodies to neurofilament proteins as well as with Lewy body (LB)- and paired helical filament-specific antibodies. The results indicate that the amygdala is severely affected by the accumulation of both neurofibrillary tangles (NFTs) and LBs in most cases of the diseases mentioned above, and that amygdala LBs have a similar epitope composition to that of LBs in the brain stem and cerebral cortex. While large numbers of both LBs and NFTs were seen in different neurons within the amygdala, these two lesions frequently occurred together in the same neurons of the amygdala. These findings are in contrast to other sites that accumulate LBs and NFTs, but rarely both lesions in the same neuron. Thus, amygdala neurons may be selectively vulnerable to developing both LBs and NFTs, and these inclusions may play a role in the massive degeneration of these neurons in AD and LB disorders of the elderly.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050454
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    Paper (German National Licenses)
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  • 8
    Electronic Resource
    Electronic Resource
    Amyloid plaques in Guam amyotrophic lateral sclerosis/ parkinsonism-dementia complex contain species of Aβ similar to those found in the amyloid plaques of Alzheimer’s disease and pathological aging (1998)
    Springer
    Acta neuropathologica 95 (1998), S. 117-122 
    Details
    ISSN: 1432-0533
    Keywords: Key words Amyloid plaques ; Amyotrophic lateral ; sclerosis/parkinsonism-dementia complex ; Guam ; End-terminus-specific anti-amyloid β protein antibodies ; N-terminal modification of amyloid β protein
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The Guamanian amyotrophic lateral sclerosis/parkinsonism-dementia complex (ALS/PDC) is characterized by abundant neurofibrillary pathology and neuron loss. In contrast to Alzheimer’s disease (AD), where extensive neurofibrillary lesions always occur with deposits of Aβ in numerous amyloid plaques, Aβ-rich amyloid plaques are absent or rare in most ALS/PDC patients. To characterize the amyloid plaques in the latter patients, we probed plaque-rich sections of their brains by immunohistochemistry using well-characterized antibodies to specific epitopes in the N and C termini of Aβ as well as to defined epitopes in hyperphosphorylated tau (PHFtau). The results indicate that the species of Aβ in the amyloid plaques of ALS/PDC patients resemble those detected in the amyloid plaques of cognitively intact subjects with pathological aging as well as patients with AD. However, the paucity of PHFtau-positive neurites in the ALS/PDC plaques suggests that they reflect pathological aging rather than AD.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050774
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    Paper (German National Licenses)
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