Ubiquilin-1 immunoreactivity is concentrated on Hirano bodies and dystrophic neurites in Alzheimer's disease brains

2013 ◽  
Vol 39 (7) ◽  
pp. 817-830 ◽  
Author(s):  
J. Satoh ◽  
H. Tabunoki ◽  
T. Ishida ◽  
Y. Saito ◽  
K. Arima
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Dystrophic Neurites ◽  
Hirano Bodies

Different Morphology of Neuritic Plaques in the Archicortex of Alzheimer’s Disease with Comorbid Synucleinopathy: A Pilot Study

2020 ◽  
Vol 17 ◽  
Author(s):  
Nikol Jankovska ◽  
Tomas Olejar ◽  
Jaromir Kukal ◽  
Radoslav Matej
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Pilot Study ◽  
Time Course ◽  
Clinical Course ◽  
Lewy Bodies ◽  
Dystrophic Neurites ◽  
Neuritic Plaques ◽  
Structural Differences ◽  
Lewy Body Variant

Background: Bulbous neuritic changes in neuritic plaques have already been described, and their possible effect on the clinical course of the disease has been discussed. OBJECTIVE: In our study, we focused on the location and density of these structures in patients with only Alzheimer’s disease (AD) and patients with AD in comorbidity with synucleinopathies. Methods: Utilizing immunohistochemistry and confocal microscopy, we evaluated differences of neocortical and archicortical neuritic plaques and the frequency of bulbous changes in the archicortex of 14 subjects with Alzheimer’s disease (AD), 10 subjects with the Lewy body variant of Alzheimer's disease (AD/DLB), and 4 subjects with Alzheimer's disease with amygdala Lewy bodies (AD/ALB). Also, the progression and density of neuritic changes over the time course of the disease were evaluated. Results: We found structural differences in bulbous dystrophic neurites more often in AD/DLB and AD/ALB than in pure AD cases. The bulbous neuritic changes were more prominent in the initial and progressive phases and were reduced in cases with a long clinical course. Conclusion: Our results indicate that there is a prominent difference in the shape and composition of neocortical and archicortical neuritic plaques and, moreover, that bulbous neuritic changes can be observed at a higher rate in AD/DLB and AD/ALB subjects compared to pure AD subjects. This observation probably reflects that these subacute changes are more easily seen in the faster clinical course of AD patients with comorbidities.

Identification and distribution of axonal dystrophic neurites in Alzheimer's disease

1993 ◽  
Vol 625 (2) ◽  
pp. 228-237 ◽  
Author(s):  
Joseph H. Su ◽  
Brian J. Cummings ◽  
Carl W. Cotman
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Dystrophic Neurites

Accumulation of cellular prion protein within dystrophic neurites of amyloid plaques in the Alzheimer's disease brain

2010 ◽  
Vol 31 (3) ◽  
pp. 208-214 ◽  
Author(s):  
Reisuke H. Takahashi ◽  
Minoru Tobiume ◽  
Yuko Sato ◽  
Tetsutaro Sata ◽  
Gunnar K. Gouras ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Prion Protein ◽  
Amyloid Plaques ◽  
Cellular Prion Protein ◽  
Dystrophic Neurites

scholarly journals Role of Cofilin in Alzheimer’s Disease

2020 ◽  
Vol 8 ◽  
Author(s):  
Qiang Wang ◽  
Wei Yuan ◽  
Xiaohang Yang ◽  
Yuan Wang ◽  
Yongfeng Li ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Plaques ◽  
Executive Dysfunction ◽  
Actin Binding ◽  
Synaptic Dysfunction ◽  
Hyperphosphorylated Tau ◽  
Hirano Bodies ◽  
Visual Spatial ◽  
Β Amyloid

Alzheimer’s disease (AD) is a degenerative neurological disease and has an inconspicuous onset and progressive development. Clinically, it is characterized by severe dementia manifestations, including memory impairment, aphasia, apraxia, loss of recognition, impairment of visual-spatial skills, executive dysfunction, and changes in personality and behavior. Its etiology is unknown to date. However, several cellular biological signatures of AD have been identified such as synaptic dysfunction, β-amyloid plaques, hyperphosphorylated tau, cofilin-actin rods, and Hirano bodies which are related to the actin cytoskeleton. Cofilin is one of the most affluent and common actin-binding proteins and plays a role in cell motility, migration, shape, and metabolism. They also play an important role in severing actin filament, nucleating, depolymerizing, and bundling activities. In this review, we summarize the structure of cofilins and their functional and regulating roles, focusing on the synaptic dysfunction, β-amyloid plaques, hyperphosphorylated tau, cofilin-actin rods, and Hirano bodies of AD.

P3-105: Abnormal Accumulation of Activated SYK in Microglia and Dystrophic Neurites in Mouse Models of Alzheimer’s Disease

2016 ◽  
Vol 12 ◽  
pp. P859-P859
Author(s):  
Jonas Schweig ◽  
David Beaulieu-Abdelahad ◽  
Yong Lin ◽  
Fiona Crawford ◽  
Daniel Paris ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Models ◽  
Dystrophic Neurites ◽  
Abnormal Accumulation

scholarly journals Diagnostic utility of quantitating neurofilament-immunoreactive Alzheimer's disease lesions.

1994 ◽  
Vol 42 (12) ◽  
pp. 1625-1634 ◽  
Author(s):  
S M de la Monte ◽  
J R Wands
Keyword(s):  
Alzheimer’S Disease ◽  
Parkinson’S Disease ◽  
Alzheimer's Disease ◽  
Parkinson's Disease ◽  
Monoclonal Antibodies ◽  
Neurofibrillary Tangles ◽  
Paired Helical Filament ◽  
Dystrophic Neurites ◽  
Associated Lesions ◽  
End Stage

The diagnosis of Alzheimer's disease (AD) neurodegeneration is based on histopathological detection of paired helical filament-associated lesions. Silver stains are routinely used but the results are fraught with intra- and interinstitutional variability. This study employed monoclonal antibodies to middle and high molecular weight neurofilament subunits in an immunohistochemical assay to assess the extent of paired helical filament-associated lesions in brains with AD, Down's syndrome plus AD lesions (AD+DN), Parkinson's disease dementia (PD), AD+PD, and normal aging changes. The densities of neurofilament-immunoreactive (NFI) cortical neurofibrillary tangles and plaques were significantly higher in AD and AD+DN than in PD and aged control brains (p < 0.001), and NFI neurofibrillary tangles and plaques were more abundant in AD and AD+DN compared with AD+PD and PD, yet all patients with AD, AD+PD, or PD died with end-stage dementia. In contrast, the densities of NFI dystrophic neurites (primarily dendrites) in cortical Layer 2 were similar among the AD, AD+DN, AD+PD, and PD groups, and all were significantly higher than control (p < 0.005). Stepwise multivariate regression analysis demonstrated significant correlations between AD diagnosis and high densities of NFI neurofibrillary tangles and plaques (p < 0.001) and between end-stage AD-type dementia and high densities of NFI dystrophic neurites (p < 0.001). This study demonstrates that the histopathological lesions correlated with AD dementia can be readily detected and quantified by immunostaining with monoclonal antibodies to phosphorylated and non-phosphorylated neurofilaments. Moreover, the findings suggest that NFI neurite pathology may be an important feature contributing to the clinically manifested AD-type dementia in individuals with Parkinson's disease.

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