Home > Riviste > Journal of Neurosurgical Sciences > Fascicoli precedenti > Articoli online first > Journal of Neurosurgical Sciences 2015 Sep 08

ULTIMO FASCICOLO
 

ARTICLE TOOLS

Estratti

JOURNAL OF NEUROSURGICAL SCIENCES

Rivista di Neurochirurgia


Indexed/Abstracted in: e-psyche, EMBASE, PubMed/MEDLINE, Neuroscience Citation Index, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 1,651


eTOC

 

Journal of Neurosurgical Sciences 2015 Sep 08

lingua: Inglese

IGF-1: an endogenous link between traumatic brain injury and AD?

Zheng P., Tong W.

Shanghai Pudong New Area People’s Hospital, Shanghai, China


PDF  


There is a growing body of evidence that the insulin-like growth factor-1 (IGF-1) is dynamically involved in the regulation of body homeostasis and glucose regulation. Traumatic brain injury (TBI) is considered to be a risk factor for Alzheimer’s disease (AD). As alterations of IGF-1 has been implicated in both TBI and AD and the IGF-1 signaling also mediates the neuronal excitability and synaptic plasticity in both diseases, we propose that IGF-1 may act as the endogenous connection between TBI and AD. Growing evidence suggests that dysfunction of this pathway contributes to the progressive loss of neurons in Alzheimer’s disease (AD), one of the most frequent neurodegenerative disorders. These findings have led to numerous studies in preclinical models of neurodegenerative disorders targeting IGF-1 signaling with currently available anti-diabetics. These studies have shown that exogenous administration of IGF-1 reverses signaling abnormalities and has neuroprotective effects. In the first part of this review, we discuss physiological functions of IGF-1 signaling pathway including its distribution within the brain and its relationship with TBI and AD. In the second part, we undertake a comprehensive overview of IGF-1 signaling in TBI and AD, respectively. We then detail targeted IGF-1 in preclinical models of neurodegeneration and the design of clinical trials that have used anti-diabetics for treating AD patients. We close with future considerations that treat relevant issues for successful translation of these encouraging preclinical results into clinical sessions.

inizio pagina

Publication History

Per citare questo articolo

Corresponding author e-mail

jojo_ras@126.com