Fr. 188.00

Diabetes, Insulin and Alzheimer's Disease

Inglese · Copertina rigida

Spedizione di solito entro 2 a 3 settimane (il titolo viene stampato sull'ordine)

Descrizione

Ulteriori informazioni

Neurons share more similarities with insulin-producing pancreatic islet cells than with any other cell type. The root of this similarity may lie in the islet's evolution from an ancestral insulin-producing neuron. The islet-neuron connection becomes less surprising as we learn more about insulin's involvement in functions far from its traditional role in mediating glucose uptake in muscle. The importance of insulin in the regulation of corporal aging has been established by the dramatic increases in longevity experienced by animals in which the adipose insulin receptor has been genetically eliminated, or in which the insulin-related daf genes have been mutated. New research suggests that, analogous to its influence on corporal aging, insulin also makes important contributions to brain aging and the expression of late-life neurodegenerative disease. Insulin plays a key role in cognition and other aspects of normal brain function. Insulin resistance induces chronic peripheral insulin elevations and is associated with reduced insulin activity both in periphery and brain. The insulin resistance syndrome underlies conditions such as Type 2 diabetes mellitus and hypertension, which are associated with age-related cognitive impairment and Alzheimer's disease.
This book discusses the mechanisms through which insulin dysregulation contributes to the development of cognitive impairment and late-life neurodegenerative disease. Given the recent pandemic of conditions associated with insulin resistance, it is imperative that we achieve a comprehensive knowledge of the mechanisms through which insulin resistance affects brain function in order to develop therapeutic strategies to address these effects.

Sommario

Insulin Action in the Brain and the Pathogenesis of Alzheimer's Disease.- The Brain-insulin Connection, Metabolic Diseases and Related Pathologies.- Insulin-Mediated Neuroplasticity in the Central Nervous System.- Stress Hormones and Neuroplasticity in the Diabetic Brain.- Diabetes and the Brain - An Epidemiologic Perspective.- Cognition in Type 2 Diabetes: Brain Imaging Correlates and Vascular and Metabolic Risk Factors.- The Relationship Between the Continuum of Elevated Adiposity, Hyperinsulinemia, and Type 2 Diabetes and Late-onset Alzheimer's Disease: An Epidemiological Perspective.- The Role of Insulin Dysregulation in Aging and Alzheimer's Disease.- Is Alzheimer's a Disorder of Ageing and Why Don't Mice get it? The Centrality of Insulin Signalling to Alzheimer's Disease Pathology.- PKC and Insulin Pathways in Memory Storage: Targets for Synaptogenesis, Anti-apoptosis, and the Treatment of AD.- Diet, Abeta Oligomers and Defective Insulin and Neurotrophic Factor Signaling in Alzheimer's Disease.- Serum IGF-I, Life Style, and Risk of Alzheimer's disease.

Riassunto

This text provides a broad survey of the role of insulin in the brain. And it discusses the mechanisms through which insulin dysregulation contributes to the development of cognitive impairment and late-life neurodegenerative disease.

Dettagli sul prodotto

Con la collaborazione di Yves Christen (Editore), Suzann Craft (Editore), Suzanne Craft (Editore)
Editore Springer, Berlin
 
Lingue Inglese
Formato Copertina rigida
Pubblicazione 22.09.2009
 
EAN 9783642042997
ISBN 978-3-642-04299-7
Pagine 218
Dimensioni 159 mm x 245 mm x 15 mm
Peso 512 g
Illustrazioni XIV, 218 p. 30 illus., 21 illus. in color.
Serie Research and Perspectives in Alzheimer's Disease
Research and Perspectives in Alzheimer's Disease
Categoria Scienze naturali, medicina, informatica, tecnica > Medicina > Branche non cliniche

Recensioni dei clienti

Per questo articolo non c'è ancora nessuna recensione. Scrivi la prima recensione e aiuta gli altri utenti a scegliere.

Scrivi una recensione

Top o flop? Scrivi la tua recensione.

Per i messaggi a CeDe.ch si prega di utilizzare il modulo di contatto.

I campi contrassegnati da * sono obbligatori.

Inviando questo modulo si accetta la nostra dichiarazione protezione dati.