The role of Ca2+ channel modulation in the neuroprotective actions of estrogen in β-amyloid protein and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) cytotoxic models

2004 ◽  
Vol 45 (1) ◽  
pp. 31-38 ◽  
Author(s):  
F Ba
Keyword(s):  
Amyloid Protein ◽  
Channel Modulation ◽  
Β Amyloid ◽  
Neuroprotective Actions

Role of the β‐amyloid protein in Alzheimer's disease

1995 ◽  
Vol 9 (5) ◽  
pp. 366-370 ◽  
Author(s):  
Sangram S. Sisodia ◽  
Donald L. Price
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Protein ◽  
Β Amyloid

scholarly journals Role of Neuroglobin in the Neuroprotective Actions of Estradiol and Estrogenic Compounds

Cells ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1907
Author(s):  
George E. Barreto ◽  
Andrew J. McGovern ◽  
Luis M. Garcia-Segura
Keyword(s):  
Sex Differences ◽  
Signaling Pathways ◽  
Glial Cell ◽  
Potential Application ◽  
Neurological Diseases ◽  
Brain Pathology ◽  
Synthetic Steroids ◽  
Neuroprotective Actions ◽  
Estrogenic Regulation

Estradiol exerts neuroprotective actions that are mediated by the regulation of a variety of signaling pathways and homeostatic molecules. Among these is neuroglobin, which is upregulated by estradiol and translocated to the mitochondria to sustain neuronal and glial cell adaptation to injury. In this paper, we will discuss the role of neuroglobin in the neuroprotective mechanisms elicited by estradiol acting on neurons, astrocytes and microglia. We will also consider the role of neuroglobin in the neuroprotective actions of clinically relevant synthetic steroids, such as tibolone. Finally, the possible contribution of the estrogenic regulation of neuroglobin to the generation of sex differences in brain pathology and the potential application of neuroglobin as therapy against neurological diseases will be examined.

scholarly journals Protective effect by T-588 against β-amyloid protein-induced microglial cell death

1999 ◽  
Vol 79 ◽  
pp. 51
Author(s):  
Takashi Fujita ◽  
Yuji Kimura ◽  
Yoko Komeda ◽  
Kazuhiro Takuma ◽  
Toshio Matsuda ◽  
...  
Keyword(s):  
Cell Death ◽  
Protective Effect ◽  
Microglial Cell ◽  
Amyloid Protein ◽  
Β Amyloid

scholarly journals Comparative studies on peptides representing the so-called tachykinin-like region of the Alzheimer Aβ peptide [Aβ(25–35)]

1998 ◽  
Vol 336 (2) ◽  
pp. 419-427 ◽  
Author(s):  
Omar M. A. EL-AGNAF ◽  
G. Brent IRVINE ◽  
Geraldine FITZPATRICK ◽  
W. Kenneth GLASS ◽  
David J. S. GUTHRIE
Keyword(s):  
Electron Microscopy ◽  
Ligand Binding ◽  
Comparative Studies ◽  
Aβ Peptide ◽  
Amyloid Protein ◽  
Binding Studies ◽  
Nk1 Receptors ◽  
Ligand Displacement ◽  
Β Amyloid

In an attempt to answer the question of whether or not the so-called tachykinin-like region of the Alzheimer β-amyloid protein [Aβ(25–35)] can act as a tachykinin, the sequences Aβ(25–35), Aβ(25–35)amide and their norleucine-35 and phenylalanine-31 analogues were synthesized. These peptides were examined with ligand binding studies, electron microscopy, CD and NMR. In all cases some differences were found between the Aβ(25–35) analogue and the corresponding Phe31 peptide. In addition, in ligand displacement studies on tachykinin NK1 receptors, only the Phe31 analogue showed activity comparable to that of genuine tachykinins. We conclude that peptides based on Aβ(25–35) but with a Phe residue at position 31 do display properties typical of a tachykinin, but that peptides with Ile at this position do not.

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