Toxic Advanced Glycation End Product-Dependent Alzheimer's Disease- Like Alternation in the Microtubule System
Curr Alzheimer Res. 2024 Feb 14. doi: 10.2174/0115672050288723240213053342. Online ahead of print.ABSTRACTType 2 diabetes mellitus (T2DM) is a risk factor for Alzheimer's Disease (AD). However, the detailed mechanism underlying T2DM-related AD remains unknown. In DM, many types of advanced glycation end products (AGEs) are formed and accumulated. In our previous study, we demonstrated that Glyceraldehyde (GA)-derived toxic Advanced Glycation End products (toxic AGEs, TAGE) strongly showed cytotoxicity against neurons and induced similar alterations to those observed in AD. Further, GA induced dysfunctional neurite outgrowt...
Source: Current Alzheimer Research - February 15, 2024 Category: Neurology Authors: Hayahide Ooi Yoshiki Koriyama Source Type: research

Toxic Advanced Glycation End Product-Dependent Alzheimer's Disease- Like Alternation in the Microtubule System
Curr Alzheimer Res. 2024 Feb 14. doi: 10.2174/0115672050288723240213053342. Online ahead of print.ABSTRACTType 2 diabetes mellitus (T2DM) is a risk factor for Alzheimer's Disease (AD). However, the detailed mechanism underlying T2DM-related AD remains unknown. In DM, many types of advanced glycation end products (AGEs) are formed and accumulated. In our previous study, we demonstrated that Glyceraldehyde (GA)-derived toxic Advanced Glycation End products (toxic AGEs, TAGE) strongly showed cytotoxicity against neurons and induced similar alterations to those observed in AD. Further, GA induced dysfunctional neurite outgrowt...
Source: Current Alzheimer Research - February 15, 2024 Category: Neurology Authors: Hayahide Ooi Yoshiki Koriyama Source Type: research

Toxic Advanced Glycation End Product-Dependent Alzheimer's Disease- Like Alternation in the Microtubule System
Curr Alzheimer Res. 2024 Feb 14. doi: 10.2174/0115672050288723240213053342. Online ahead of print.ABSTRACTType 2 diabetes mellitus (T2DM) is a risk factor for Alzheimer's Disease (AD). However, the detailed mechanism underlying T2DM-related AD remains unknown. In DM, many types of advanced glycation end products (AGEs) are formed and accumulated. In our previous study, we demonstrated that Glyceraldehyde (GA)-derived toxic Advanced Glycation End products (toxic AGEs, TAGE) strongly showed cytotoxicity against neurons and induced similar alterations to those observed in AD. Further, GA induced dysfunctional neurite outgrowt...
Source: Current Alzheimer Research - February 15, 2024 Category: Neurology Authors: Hayahide Ooi Yoshiki Koriyama Source Type: research

Toxic Advanced Glycation End Product-Dependent Alzheimer's Disease- Like Alternation in the Microtubule System
Curr Alzheimer Res. 2024 Feb 14. doi: 10.2174/0115672050288723240213053342. Online ahead of print.ABSTRACTType 2 diabetes mellitus (T2DM) is a risk factor for Alzheimer's Disease (AD). However, the detailed mechanism underlying T2DM-related AD remains unknown. In DM, many types of advanced glycation end products (AGEs) are formed and accumulated. In our previous study, we demonstrated that Glyceraldehyde (GA)-derived toxic Advanced Glycation End products (toxic AGEs, TAGE) strongly showed cytotoxicity against neurons and induced similar alterations to those observed in AD. Further, GA induced dysfunctional neurite outgrowt...
Source: Current Alzheimer Research - February 15, 2024 Category: Neurology Authors: Hayahide Ooi Yoshiki Koriyama Source Type: research

Toxic Advanced Glycation End Product-Dependent Alzheimer's Disease- Like Alternation in the Microtubule System
Curr Alzheimer Res. 2024 Feb 14. doi: 10.2174/0115672050288723240213053342. Online ahead of print.ABSTRACTType 2 diabetes mellitus (T2DM) is a risk factor for Alzheimer's Disease (AD). However, the detailed mechanism underlying T2DM-related AD remains unknown. In DM, many types of advanced glycation end products (AGEs) are formed and accumulated. In our previous study, we demonstrated that Glyceraldehyde (GA)-derived toxic Advanced Glycation End products (toxic AGEs, TAGE) strongly showed cytotoxicity against neurons and induced similar alterations to those observed in AD. Further, GA induced dysfunctional neurite outgrowt...
Source: Current Alzheimer Research - February 15, 2024 Category: Neurology Authors: Hayahide Ooi Yoshiki Koriyama Source Type: research

Toxic Advanced Glycation End Product-Dependent Alzheimer's Disease- Like Alternation in the Microtubule System
Curr Alzheimer Res. 2024 Feb 14. doi: 10.2174/0115672050288723240213053342. Online ahead of print.ABSTRACTType 2 diabetes mellitus (T2DM) is a risk factor for Alzheimer's Disease (AD). However, the detailed mechanism underlying T2DM-related AD remains unknown. In DM, many types of advanced glycation end products (AGEs) are formed and accumulated. In our previous study, we demonstrated that Glyceraldehyde (GA)-derived toxic Advanced Glycation End products (toxic AGEs, TAGE) strongly showed cytotoxicity against neurons and induced similar alterations to those observed in AD. Further, GA induced dysfunctional neurite outgrowt...
Source: Current Alzheimer Research - February 15, 2024 Category: Neurology Authors: Hayahide Ooi Yoshiki Koriyama Source Type: research

Toxic Advanced Glycation End Product-Dependent Alzheimer's Disease- Like Alternation in the Microtubule System
Curr Alzheimer Res. 2024 Feb 14. doi: 10.2174/0115672050288723240213053342. Online ahead of print.ABSTRACTType 2 diabetes mellitus (T2DM) is a risk factor for Alzheimer's Disease (AD). However, the detailed mechanism underlying T2DM-related AD remains unknown. In DM, many types of advanced glycation end products (AGEs) are formed and accumulated. In our previous study, we demonstrated that Glyceraldehyde (GA)-derived toxic Advanced Glycation End products (toxic AGEs, TAGE) strongly showed cytotoxicity against neurons and induced similar alterations to those observed in AD. Further, GA induced dysfunctional neurite outgrowt...
Source: Current Alzheimer Research - February 15, 2024 Category: Neurology Authors: Hayahide Ooi Yoshiki Koriyama Source Type: research

Toxic Advanced Glycation End Product-Dependent Alzheimer's Disease- Like Alternation in the Microtubule System
Curr Alzheimer Res. 2024 Feb 14. doi: 10.2174/0115672050288723240213053342. Online ahead of print.ABSTRACTType 2 diabetes mellitus (T2DM) is a risk factor for Alzheimer's Disease (AD). However, the detailed mechanism underlying T2DM-related AD remains unknown. In DM, many types of advanced glycation end products (AGEs) are formed and accumulated. In our previous study, we demonstrated that Glyceraldehyde (GA)-derived toxic Advanced Glycation End products (toxic AGEs, TAGE) strongly showed cytotoxicity against neurons and induced similar alterations to those observed in AD. Further, GA induced dysfunctional neurite outgrowt...
Source: Current Alzheimer Research - February 15, 2024 Category: Neurology Authors: Hayahide Ooi Yoshiki Koriyama Source Type: research

Toxic Advanced Glycation End Product-Dependent Alzheimer's Disease- Like Alternation in the Microtubule System
Curr Alzheimer Res. 2024 Feb 14. doi: 10.2174/0115672050288723240213053342. Online ahead of print.ABSTRACTType 2 diabetes mellitus (T2DM) is a risk factor for Alzheimer's Disease (AD). However, the detailed mechanism underlying T2DM-related AD remains unknown. In DM, many types of advanced glycation end products (AGEs) are formed and accumulated. In our previous study, we demonstrated that Glyceraldehyde (GA)-derived toxic Advanced Glycation End products (toxic AGEs, TAGE) strongly showed cytotoxicity against neurons and induced similar alterations to those observed in AD. Further, GA induced dysfunctional neurite outgrowt...
Source: Current Alzheimer Research - February 15, 2024 Category: Neurology Authors: Hayahide Ooi Yoshiki Koriyama Source Type: research

Microglia PTK2B/Pyk2 in the Pathogenesis of Alzheimer's Disease
Curr Alzheimer Res. 2024 Feb 6. doi: 10.2174/0115672050299004240129051655. Online ahead of print.ABSTRACTAlzheimer's disease (AD) is a highly hereditary disease with complex genetic susceptibility factors. Extensive genome-wide association studies have established a distinct susceptibility link between the protein tyrosine kinase 2β (PTK2B) gene and late-onset Alzheimer's disease (LOAD), but the specific pathogenic mechanisms remain incompletely understood. PTK2B is known to be expressed in neurons, and recent research has revealed its more important significance in microglia. Elucidating the role of PTK2B high expression...
Source: Current Alzheimer Research - February 7, 2024 Category: Neurology Authors: Yun Guo Cheng-Kun Sun Lian Tang Meng-Shan Tan Source Type: research

Follow-up Comparisons of Two Plasma Biomarkers of Alzheimer's Disease, Neurofilament Light Chain, and Oligomeric A β: A Pilot Study
CONCLUSION: This study shows that only in participants with SCD and MCI, not including AD dementia, can MDS-OAß predict the longitudinal cognitive decline measured by follow-up MMSE. Changes of NfL, not MDS-OAß, parallel the changes of MMSE. Further studies with larger samples and longer durations could strengthen these results.PMID:38299421 | DOI:10.2174/0115672050284054240119101834 (Source: Current Alzheimer Research)
Source: Current Alzheimer Research - February 1, 2024 Category: Neurology Authors: Yong Soo Shim Source Type: research

Association of Autoimmune Disorders and Disease-modifying Antirheumatic Drugs with the Risk of Alzheimer's and/or Dementia: A Population Study Using Medicare Beneficiary Data
CONCLUSION: This study provides evidence of an association between RA and increased risk of AD and/or dementia. The findings suggest that DMARD use may have a protective effect against the development of AD and/or dementia in patients with an autoimmune disorder.PMID:38288824 | DOI:10.2174/0115672050289966240110041616 (Source: Current Alzheimer Research)
Source: Current Alzheimer Research - January 30, 2024 Category: Neurology Authors: Qian Ding Jennifer Lamberts Alison M Konieczny Tyler B Bringedahl Kiara Y Torres Garcia Source Type: research

Development and Optimization of a Target Engagement Model of Brain IDO Inhibition for Alzheimer's Disease
CONCLUSION: This LPS-based model of IDO1 target engagement is a useful tool that can be used in the development of brain penetrant IDO1 inhibitors for AD. A limitation of the present study is the lack of quantification of potential clinically relevant biomarkers in this model, which could be addressed in future studies.PMID:38288825 | DOI:10.2174/0115672050283199240111111801 (Source: Current Alzheimer Research)
Source: Current Alzheimer Research - January 30, 2024 Category: Neurology Authors: Kurt R Stover Paul M Stafford Andreea C Damian Jagadeesh P Pasangulapati Jake Goodwin-Tindall Luc ía M López Vásquez Sanghyun Lee Seung-Pil Yang Mark A Reed Christopher J Barden Donald F Weaver Source Type: research

Interactions of Polyphenolic Gallotannins with Amyloidogenic Polypeptides Associated with Alzheimer's Disease: From Molecular Insights to Physiological Significance
Curr Alzheimer Res. 2023;20(9):603-617. doi: 10.2174/0115672050277001231213073043.ABSTRACTPolyphenols are natural compounds abundantly found in plants. They are known for their numerous benefits to human health, including antioxidant properties and anti-inflammatory activities. Interestingly, many studies have revealed that polyphenols can also modulate the formation of amyloid fibrils associated with disease states and can prevent the formation of cytotoxic oligomer species. In this review, we underline the numerous effects of four hydrolysable gallotannins (HGTs) with high conformational flexibility, low toxicity, and mu...
Source: Current Alzheimer Research - January 25, 2024 Category: Neurology Authors: Jihane Khalifa Steve Bourgault Roger Gaudreault Source Type: research

Neuropharmacological Study on Capsaicin in Scopolamine-injected Mice
CONCLUSION: The experiential neuroprotective effect of capsaicin through the restoration of mitochondrial functions, antioxidant effects, and modulation of pro-inflammatory cytokines makes it a promising candidate for further drug development through clinical setup.PMID:38213170 | DOI:10.2174/0115672050286225231230130613 (Source: Current Alzheimer Research)
Source: Current Alzheimer Research - January 12, 2024 Category: Neurology Authors: Sakshi Tyagi Ajit Kumar Thakur Source Type: research