scholarly journals Displacement of corticotropin releasing factor from its binding protein as a possible treatment for Alzheimer's disease

Nature ◽  
1995 ◽  
Vol 378 (6554) ◽  
pp. 284-287 ◽  
Author(s):  
Dominic P. Behan ◽  
Stephen C. Heinrichs ◽  
Juan C. Troncoso ◽  
Xin-Jun Liu ◽  
Claudia H. Kawas ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Binding Protein ◽  
Corticotropin Releasing Factor

scholarly journals Corticotropin releasing factor-binding protein (CRF-BP) as a potential new therapeutic target in Alzheimer’s disease and stress disorders

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Dorien Vandael ◽  
Natalia V. Gounko
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neurodegenerative Diseases ◽  
Therapeutic Target ◽  
Life Stress ◽  
Binding Protein ◽  
Critical Role ◽  
Treatment Strategies ◽  
Corticotropin Releasing Factor ◽  
Stress Disorders

Abstract Alzheimer’s disease is the most common cause of dementia and one of the most complex human neurodegenerative diseases. Numerous studies have demonstrated a critical role of the environment in the pathogenesis and pathophysiology of the disease, where daily life stress plays an important role. A lot of epigenetic studies have led to the conclusion that chronic stress and stress-related disorders play an important part in the onset of neurodegenerative disorders, and an enormous amount of research yielded valuable discoveries but has so far not led to the development of effective treatment strategies for Alzheimer’s disease. Corticotropin-releasing factor (CRF) is one of the major hormones and at the same time a neuropeptide acting in stress response. Deregulation of protein levels of CRF is involved in the pathogenesis of Alzheimer’s disease, but little is known about the precise roles of CRF and its binding protein, CRF-BP, in neurodegenerative diseases. In this review, we summarize the key evidence for and against the involvement of stress-associated modulation of the CRF system in the pathogenesis of Alzheimer’s disease and discuss how recent findings could lead to new potential treatment possibilities in Alzheimer’s disease by using CRF-BP as a therapeutic target.

P1-068: Association between vitamin D binding protein (VDBP) haplotype and late-onset Alzheimer's disease

2013 ◽  
Vol 9 ◽  
pp. P177-P177
Author(s):  
Omur Selin Araz ◽  
Erdinc Dursun ◽  
Duygu Gezen-Ak ◽  
Hasmet Hanagasi ◽  
Basar Bilgiç ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Vitamin D ◽  
Late Onset ◽  
Binding Protein ◽  
Vitamin D Binding Protein

P4-122 Genetic association of an APP binding protein gene with late onset Alzheimer's disease

2004 ◽  
Vol 25 ◽  
pp. S510
Author(s):  
Yonghong Li ◽  
Paul Hollingworth ◽  
Pamela Moore ◽  
Catherine Foy ◽  
Nicola Archer ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Genetic Association ◽  
Protein Gene ◽  
Late Onset ◽  
Binding Protein ◽  
Binding Protein Gene

scholarly journals Corticotropin-Releasing Factor Receptor-1 Antagonism Reduces Oxidative Damage in an Alzheimer's Disease Transgenic Mouse Model

2015 ◽  
Vol 45 (2) ◽  
pp. 639-650 ◽  
Author(s):  
Cheng Zhang ◽  
Ching-Chang Kuo ◽  
Setareh H. Moghadam ◽  
Louise Monte ◽  
Kenner C. Rice ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Oxidative Damage ◽  
Transgenic Mouse ◽  
Transgenic Mouse Model ◽  
Corticotropin Releasing Factor

Smuggle tau through a secret(ory) pathway

2021 ◽  
Vol 478 (14) ◽  
pp. 2921-2925
Author(s):  
Hao Xu (徐昊)
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neurodegenerative Diseases ◽  
Recent Work ◽  
Molecular Mechanisms ◽  
Binding Protein ◽  
Nerve Cells ◽  
Transmembrane Domains ◽  
Tau Pathology ◽  
Microtubule Binding

Secretion of misfolded tau, a microtubule-binding protein enriched in nerve cells, is linked to the progression of tau pathology. However, the molecular mechanisms underlying tau secretion are poorly understood. Recent work by Lee et al. [Biochemical J. (2021) 478: 1471–1484] demonstrated that the transmembrane domains of syntaxin6 and syntaxin8 could be exploited for tau release, setting a stage for testing a novel hypothesis that has profound implications in tauopathies (e.g. Alzheimer's disease, FTDP-17, and CBD/PSP) and other related neurodegenerative diseases. The present commentary highlights the importance and limitations of the study, and discusses opportunities and directions for future investigations.

O2-04-06: GRB-associated binding protein 2 (GAB2) interacts with APOE to alter risk of late-onset Alzheimer's disease

2009 ◽  
Vol 5 (4S_Part_4) ◽  
pp. P111-P111
Author(s):  
Gary W. Beecham ◽  
Adam C. Naj ◽  
Guiqing Cai ◽  
Yuji Kajiwara ◽  
Vahram Haroutunian ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Late Onset ◽  
Binding Protein
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