scholarly journals A small molecule transcription factor EB activator ameliorates beta‐amyloid precursor protein and Tau pathology in Alzheimer's disease models

Aging Cell ◽  
2019 ◽  
Vol 19 (2) ◽  
Author(s):  
Ju‐Xian Song ◽  
Sandeep Malampati ◽  
Yu Zeng ◽  
Siva Sundara Kumar Durairajan ◽  
Chuan‐Bin Yang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transcription Factor ◽  
Amyloid Precursor Protein ◽  
Small Molecule ◽  
Beta Amyloid ◽  
Precursor Protein ◽  
Disease Models ◽  
Tau Pathology ◽  
Transcription Factor Eb

Understanding the structural requirements of cyclic sulfone hydroxyethylamines as hBACE1 inhibitors against Aβ plaques in Alzheimer's disease: a predictive QSAR approach

RSC Advances ◽  
2016 ◽  
Vol 6 (34) ◽  
pp. 28171-28186 ◽  
Author(s):  
Pravin Ambure ◽  
Kunal Roy
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Precursor Protein ◽  
Beta Amyloid ◽  
Precursor Protein ◽  
Structural Requirements ◽  
Amyloid Aβ

Beta (β)-site amyloid precursor protein cleaving enzyme 1 (BACE1) is one of the most important targets in Alzheimer's disease (AD), which is responsible for production and accumulation of beta amyloid (Aβ).

scholarly journals Beta-Amyloid Precursor Protein (βAPP) Processing in Alzheimer’s Disease (AD) and Age-Related Macular Degeneration (AMD)

2014 ◽  
Vol 52 (1) ◽  
pp. 533-544 ◽  
Author(s):  
Yuhai Zhao ◽  
Surjyadipta Bhattacharjee ◽  
Brandon M. Jones ◽  
James M. Hill ◽  
Christian Clement ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Precursor Protein ◽  
Macular Degeneration ◽  
Beta Amyloid ◽  
Precursor Protein ◽  
Age Related Macular Degeneration ◽  
Age Related

The β-Secretase Enzyme BACE1: A Biochemical Enigma for Alzheimer’s Disease

2020 ◽  
Vol 19 (3) ◽  
pp. 184-194
Author(s):  
Hirak Shah ◽  
Ashish Patel ◽  
Vruti Parikh ◽  
Afzal Nagani ◽  
Bhargav Bhimani ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Precursor Protein ◽  
Small Molecule ◽  
Normal Function ◽  
Precursor Protein ◽  
Voltage Gated ◽  
Small Series ◽  
The Brain ◽  
Translational Level

Beta site amyloid precursor protein cleaving enzyme 1 (BACE1) is a rational target in Alzheimer’s Disease (AD) drug development due to its role in amyloidogenic cleavage of Amyloid Precursor Protein (APP) in generating Amyloid β (Aβ). This β-secretase cleaves not only Amyloid Precursor Protein (APP) and its homologues, but also small series of substrates including neuregulin and β subunit of voltage-gated sodium channel that play a very important role in the development and normal function of the brain. Moreover, BACE1 is modulated at the post-translational level by several factors that are associated with both physiological and pathological functions. Since the discovery of BACE1 over a decade ago, medicinal chemistry and pharmacokinetics of BACE1 small molecule inhibitors have proven challenging for the treatment of Alzheimer’s disease.

scholarly journals A Possible Role for Cathepsins D, E, and B in the Processing of beta-amyloid Precursor Protein in Alzheimer's Disease

1997 ◽  
Vol 244 (2) ◽  
pp. 414-425 ◽  
Author(s):  
Elaine A. Mackay ◽  
Anne Ehrhard ◽  
Marc Moniatte ◽  
Chantal Guenet ◽  
Chantal Tardif ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Precursor Protein ◽  
Beta Amyloid ◽  
Precursor Protein

scholarly journals Intensive protein synthesis in neurons and phosphorylation of beta-amyloid precursor protein and tau-protein are triggering factors of neuronal amyloidosis and Alzheimer's disease

2013 ◽  
Vol 59 (2) ◽  
pp. 144-170 ◽  
Author(s):  
A.V. Maltsev ◽  
N.V. Dovidchenko ◽  
V.K. Uteshev ◽  
V.V. Sokolik ◽  
O.M. Shtang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Protein Synthesis ◽  
Amyloid Precursor Protein ◽  
Tau Protein ◽  
Beta Amyloid ◽  
Precursor Protein ◽  
Tau Proteins ◽  
Neuron Death ◽  
Protective Mechanisms

Recently the studies of Alzheimer’s disease have become particularly actual and have attracted scientists from all over the world to this problem as a result of dissemination of this dangerous disorder. The reason for such pathogenesis is not known, but the final image, for the first time obtained on microscopic brain sections from patients with this disease more than a hundred years ago, is well known to clinicists. This is the deposition of Ab amyloid in the brain tissue of senile plaques and fibrils. Many authors suppose that the deposition of beta-amyloid provokes secondary neuronal changes which are the reason of neuron death. Other authors associate the death of neurons with hyperphosphorylation of tau-proteins which form neurofibrillar coils inside nerve cells and lead to their death. For creation of methods of preclinical diagnostics and effective treatment of Alzheimer’s disease novel knowledge is required on the nature of triggering factors of sporadic isoforms of Alzheimer’s disease, on cause-effect relationships of phosphorylation of amyloid precursor protein with formation of pathogenic beta-amyloids, on the relationship with these factors of hyperphosphorylation of tau-protein and neuron death. In this review we analyze the papers describing the increasing of intensity of biosynthesis in neurons in normal conditions and under the stress, the possibility of development of energetic unbalanced neurons and activation of their protective systems. Phosphorylation and hyperphosphorylation of tau-proteins is also tightly connected with protective mechanisms of cells and with processes of evacuation of phosphates, adenosine mono-phosphates and pyrophosphates from the region of protein synthesis. Upon long and high intensity of protein synthesis the protective mechanisms are overloaded and the complementarity of metabolitic processes is disturbed. This results in dysfunction of neurons, transport collapse, and neuron death.

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