Neuronal Signal Transduction and Alzheimer’s Disease. Based on a symposium held in Cork, Ireland, September 1999. Biochemical Society Symposium, Volume 67. Organized and Edited by C  O’Neill and , B  Anderton. London: Portland Press. £65.00. xii + 213 p; ill.; subject index. ISBN: 1–85578–133–6. 2001.

2002 ◽  
Vol 77 (3) ◽  
pp. 357-357
Author(s):  
René Etcheberrigaray
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Signal Transduction ◽  
Society Symposium ◽  
Neuronal Signal

Dysfunctional intracellular calcium homoeostasis: a central cause of neurodegeneration in Alzheimer's disease

2001 ◽  
Vol 67 ◽  
pp. 177-194 ◽  
Author(s):  
Cora O'Neill ◽  
Richard F. Cowburn ◽  
Willy L. Bonkale ◽  
Thomas G. Ohm ◽  
Johan Fastbom ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Signal Transduction ◽  
Intracellular Calcium ◽  
Clinical Symptoms ◽  
Cellular Events ◽  
Hyperphosphorylated Tau Protein ◽  
Progressive Neurodegeneration ◽  
Signal Transduction Event ◽  
Neuronal Signal

The clinical symptoms of all forms of Alzheimer's disease (AD) result from a slowly progressive neurodegeneration that is associated with the excessive deposition of ϐ-amyloid (Aϐ) in plaques and in the cerebrovasculature, and the formation of intraneuronal neurofibrillary tangles, which are composed primarily of abnormally hyperphosphorylated tau protein. The sequence of cellular events that cause this pathology and neurodegeneration is unknown. It is, however, most probably linked to neuronal signal transduction systems that become misregulated in the brains of certain individuals, causing excessive Aϐ to be formed and/or deposited, tau to become aggregated and hyperphosphorylated and neurons to degenerate. We hypothesize that a progressive alteration in the ability of neurons to regulate intracellular calcium, particularly at the level of the endoplasmic reticulum, is a crucial signal transduction event that is linked strongly to the initiation and development of AD pathology. In this chapter we will discuss the key findings that lend support to this hypothesis.

The Phosphoinositide Signal Transduction Pathway in the Pathogenesis of Alzheimer’s Disease

2018 ◽  
Vol 15 (4) ◽  
pp. 355-362 ◽  
Author(s):  
Vincenza Rita Lo Vasco
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Signal Transduction ◽  
Membrane Trafficking ◽  
Hormone Secretion ◽  
Signal Transduction Pathway ◽  
Brain Morphology ◽  
Signal Transduction Pathways ◽  
Transduction Pathway ◽  
Cell Functions

Background: During aging and in age-associated disorders, such as Alzheimer's Disease (AD), learning abilities decline. Probably, disturbances in signal transduction in brain cells underlie the cognitive decline. The phosphorylation/dephosphorylation imbalance occurring in degenerating neurons was recently related to abnormal activity of one or more signal transduction pathways. AD is known to be associated with altered neuronal Ca<sup>2+</sup> homeostasis, as Ca<sup>2+</sup> accumulates in affected neurons leading to functional impairment. It is becoming more and more evident the involvement of signal transduction pathways acting upon Ca<sup>2+</sup> metabolism and phosphorylation regulation of proteins. A growing interest raised around the role of signal transduction systems in a number of human diseases including neurodegenerative diseases, with special regard to the systems related to the phosphoinositide (PI) pathway and AD. The PI signal transduction pathway plays a crucial role, being involved in a variety of cell functions, such as hormone secretion, neurotransmitter signal transduction, cell growth, membrane trafficking, ion channel activity, cytoskeleton regulation, cell cycle control, apoptosis, cell and tissue polarity, and contributes to regulate the Ca<sup>2+</sup> levels in the nervous tissue. Conclusion: A number of observations indicated that PI-specific phospholipase C (PLC) enzymes might be involved in the alteration of neurotransmission. To understand the role and the timing of action of the signalling pathways recruited during the brain morphology changes during the AD progression might help to elucidate the aetiopathogenesis of the disease, paving the way to prognosis refinement and/or novel molecular therapeutic strategies.

Disturbances in signal transduction mechanisms in Alzheimer's disease

1995 ◽  
Vol 149-150 (1) ◽  
pp. 287-292 ◽  
Author(s):  
Christopher J. Fowler ◽  
Richard F. Cowburn ◽  
Anita Garlind ◽  
Bengt Winblad ◽  
Cora O'Neill
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Signal Transduction ◽  
Transduction Mechanisms

Signal Transduction in Alzheimer’s Disease

Neurosignals ◽  
2002 ◽  
Vol 11 (5) ◽  
pp. 235-235 ◽  
Author(s):  
Mark A. Smith ◽  
Xiongwei Zhu ◽  
George Perry
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Signal Transduction

Ionic and signal transduction alterations in Alzheimer’s disease

1999 ◽  
Vol 20 (2-3) ◽  
pp. 93-109 ◽  
Author(s):  
René Etcheberrigaray ◽  
Seetha Bhagavan
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Signal Transduction

scholarly journals Rapid, quantitative therapeutic screening for Alzheimer's enzymes enabled by optimal signal transduction with transistors

The Analyst ◽  
2020 ◽  
Vol 145 (8) ◽  
pp. 2925-2936
Author(s):  
Son T. Le ◽  
Michelle A. Morris ◽  
Antonio Cardone ◽  
Nicholas B. Guros ◽  
Jeffery B. Klauda ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Signal Transduction ◽  
Field Effect ◽  
Field Effect Transistors ◽  
Therapeutic Molecules ◽  
Optimal Signal

Commercially sourced silicon field-effect transistors enable sensitive measurements of small therapeutic molecules that regulate enzymes implicated in Alzheimer's disease.

P3-036: Rage signal transduction and implications for neuroinflammation in Alzheimer's disease

2015 ◽  
Vol 11 (7S_Part_13) ◽  
pp. P632-P632
Author(s):  
Julia Derk ◽  
Rosa Rosario ◽  
Paul Mathews ◽  
Ann Marie Schmidt
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Signal Transduction
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