scholarly journals Detection of hyperphosphorylated tau protein and α-synuclein in spinal cord of patients with Alzheimer’s disease

2016 ◽  
pp. 445 ◽  
Author(s):  
Luning Wang ◽  
Yanjun Guo ◽  
Mingwei Zhu ◽  
Honghong Zhang ◽  
Yazhuo Hu ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Tau Protein ◽  
Alpha Synuclein ◽  
Hyperphosphorylated Tau ◽  
Hyperphosphorylated Tau Protein

scholarly journals LRRK2, alpha-synuclein, and tau: partners in crime or unfortunate bystanders?

2019 ◽  
Vol 47 (3) ◽  
pp. 827-838 ◽  
Author(s):  
Tiago Fleming Outeiro ◽  
Kirsten Harvey ◽  
Antonio Dominguez-Meijide ◽  
Ellen Gerhardt
Keyword(s):  
Enzymatic Activity ◽  
Tau Protein ◽  
Lewy Bodies ◽  
Alpha Synuclein ◽  
Hyperphosphorylated Tau ◽  
Lewy Neurites ◽  
Hyperphosphorylated Tau Protein ◽  
Genes Encoding ◽  
Novel Targets ◽  
Domain Protein

Abstract The identification of genetic forms of Parkinson's disease (PD) has tremendously expanded our understanding of the players and mechanisms involved. Mutations in the genes encoding for alpha-synuclein (aSyn), LRRK2, and tau have been associated with familial and sporadic forms of the disease. aSyn is the major component of Lewy bodies and Lewy neurites, which are pathognomonic protein inclusions in PD. Hyperphosphorylated tau protein accumulates in neurofibrillary tangles in the brains of Alzheimer's disease patients but is also seen in the brains of PD patients. LRRK2 is a complex multi-domain protein with kinase and GTPase enzymatic activity. Since aSyn and tau are phosphoproteins, we review the possible interplay between the three proteins. Understanding the interplay between LRRK2, aSyn and tau is extremely important, as this may enable the identification of novel targets and pathways for therapeutic intervention.

scholarly journals Neuronal Deposition of Amyloid-β Oligomers and Hyperphosphorylated Tau Is Closely Connected with Cognitive Dysfunction in Aged Dogs

2021 ◽  
pp. 1-12
Author(s):  
Umma Habiba ◽  
Makiko Ozawa ◽  
James K. Chambers ◽  
Kazuyuki Uchida ◽  
Joseph Descallar ◽  
...  
Keyword(s):  
Cognitive Dysfunction ◽  
Tau Protein ◽  
Senile Plaques ◽  
Amyloid Β ◽  
Hyperphosphorylated Tau ◽  
Diffuse Type ◽  
Hippocampal Region ◽  
Immunofluorescence Analysis ◽  
Relevant Model ◽  
Hyperphosphorylated Tau Protein

Background: Canine cognitive dysfunction (CCD) is a progressive syndrome recognized in mature to aged dogs with a variety of neuropathological changes similar to human Alzheimer’s disease (AD), for which it is thought to be a good natural model. However, the presence of hyperphosphorylated tau protein (p-Tau) in dogs with CCD has only been demonstrated infrequently. Objective: The aim of the present study was to investigate the presence of p-Tau and amyloid-β oligomer (Aβo) in cerebral cortex and hippocampus of dogs with CCD, with focus on an epitope retrieval protocol to unmask p-Tau. Methods: Immunohistochemical and immunofluorescence analysis of the cortical and hippocampal regions of five CCD-affected and two nondemented aged dogs using 4G8 anti-Aβp, anti-Aβ 1 - 42 nanobody (PrioAD13) and AT8 anti-p-Tau (Ser202, Thr205) antibody were used to demonstrate the presence of Aβ plaques (Aβp) and Aβ 1 - 42 oligomers and p-Tau deposits, respectively. Results: The extracellular Aβ senile plaques were of the diffuse type which lack the dense core normally seen in human AD. While p-Tau deposits displayed a widespread pattern and closely resembled the typical human neuropathology, they did not co-localize with the Aβp. Of considerable interest, however, widespread intraneuronal deposition of Aβ 1 - 42 oligomers were exhibited in the frontal cortex and hippocampal region that co-localized with p-Tau. Conclusion: Taken together, these findings reveal further shared neuropathologic features of AD and CCD, supporting the case that aged dogs afflicted with CCD offer a relevant model for investigating human AD.

Pick's disease: hyperphosphorylated tau protein segregates to the somatoaxonal compartment

1996 ◽  
Vol 92 (6) ◽  
pp. 588-596 ◽  
Author(s):  
A. Probst ◽  
M. Tolnay ◽  
D. Langui ◽  
M. Goedert ◽  
M. G. Spillantini
Keyword(s):  
Tau Protein ◽  
Pick's Disease ◽  
Hyperphosphorylated Tau ◽  
Pick’S Disease ◽  
Hyperphosphorylated Tau Protein
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