Gerstmann-Str�ussler syndrome ? A variant type: amyloid plaques and Alzheimer's neurofibrillary tangles in cerebral cortex

1992 ◽  
Vol 84 (1) ◽  
pp. 15-23 ◽  
Author(s):  
Naoji Amano ◽  
Saburo Yagishita ◽  
Susumu Yokoi ◽  
Yoji Itoh ◽  
Jun Kinoshita ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Neurofibrillary Tangles ◽  
Amyloid Plaques ◽  
Variant Type ◽  
Alzheimer's Neurofibrillary Tangles

scholarly journals Cucumber Shaped and 35 nm Particles in Creutzfeldt-Jakob Disease

1975 ◽  
Vol 2 (3) ◽  
pp. 203-207 ◽  
Author(s):  
Dikran S. Horoupian ◽  
R.T. Ross
Keyword(s):  
Neurofibrillary Tangles ◽  
Amyloid Plaques ◽  
Jakob Disease ◽  
Alzheimer's Neurofibrillary Tangles

SUMMARY:A 63 year old female with the ataxic form of Creutzfeldt-Jakob disease (CJD) is presented. In addition to amyloid plaques which were not associated with Alzheimer’s neurofibrillary tangles, rare profiles similar to those reported in Scrapie were also seen. To our knowledge, these profiles have never been observed in CJD and their presence in this condition adds a further morphologic similarity between the human and animal forms of subacute spongiform “viral” encephalopathies.

SIRT1 Regulates Tau Expression and Tau Synaptic Pathology

2021 ◽  
pp. 1-10
Author(s):  
Xiaomin Yin ◽  
Zheng Zhou ◽  
Yanyan Qiu ◽  
Xing Fan ◽  
Chenhao Zhao ◽  
...  
Keyword(s):  
Neurofibrillary Tangles ◽  
Dendritic Spine ◽  
Amyloid Plaques ◽  
Transcriptional Level ◽  
Spine Morphology ◽  
Protein Levels ◽  
Dendritic Spine Morphology ◽  
Synaptic Pathology ◽  
Factor C ◽  
Tau Expression

Background: Amyloid plaques and neurofibrillary tangles are two pathological hallmarks of Alzheimer’s disease (AD). However, synaptic deficits occur much earlier and correlate stronger with cognitive decline than amyloid plaques and neurofibrillary tangles. Mislocalization of tau is an early hallmark of neurodegeneration and precedes aggregations. Sirtuin type 1 (SIRT1) is a deacetylase which acts on proteins including transcriptional factors and associates closely with AD. Objective: The present study investigated the association between SIRT1 and tau expression in cells and in mice brains. Methods: Western blot was performed to detected tau, SIRT1, C/EBPα, and GAPDH protein levels. Immunological fluorescence assay was used to assess tau localization in primary cortical neuronal cells. Golgi staining was performed to evaluated dendritic spine morphology in mice brains. Results: In the present study, we found that SIRT1 negatively regulates expression of tau at the transcriptional level through transcriptional factor C/EBPα. Inhibition of the activity of SIRT1 limits the distribution of tau to the neurites. In the meantime, the alteration of dendritic spine morphology is also observed in the brains of SIRT1+/– mice. Conclusion: SIRT1 may be a potential drug target for early intervention in AD.

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