Is insulin-like growth factor-1 involved in Parkinson's disease development?

• Published in: Journal of translational medicine Vol. 18; no. 1; p. 70
• Main Authors: Castilla-Cortázar, Inma, Aguirre, Gabriel A, Femat-Roldán, Giovana, Martín-Estal, Irene, Espinosa, Luis
• Format: Journal Article
• Language: English
• Published: England BioMed Central Ltd 11.02.2020; BioMed Central; BMC
• Subjects: Age; Aging; Akinesia; Animal cognition; Antioxidants; Antioxidants (Nutrients); Anxiety; Apoptosis; Autocrine signalling; Brain; Cardiotonic agents; Central nervous system; Depression (Mood disorder); Development and progression; Disease; Diseases; Dopamine; Dopamine receptors; Estrogens; Female; Gender differences; Health aspects; Homeostasis; Hormones; Humans; IGF-1; Insulin; Insulin-Like Growth Factor I; Movement disorders; Neostriatum; Neurodegeneration; Neurodegenerative diseases; Neurons; Neuroprotection; Olfaction disorders; Oxidative stress; Paracrine signalling; Parkinson Disease; Parkinson's disease; Pathogenesis; Phenols (Class of compounds); Posture; Review; Risk factors; Sex hormones; Short term memory; Sleep; Substantia nigra; Tremor; Womens health; Mexico; Aging; IGF-1; Dopamine; Estrogens; Parkinson’s disease; Central nervous system
• ISSN: 1479-5876; 1479-5876
• DOI: 10.1186/s12967-020-02223-0

Parkinson's disease (PD) is a neurodegenerative disorder that results in the death of dopaminergic neurons within the substantia nigra pars compacta and the reduction in dopaminergic control over striatal output neurons, leading to a movement disorder most commonly characterized by akinesia or bradykinesia, rigidity and tremor. Also, PD is less frequently depicted by sensory symptoms (pain and tingling), hyposmia, sleep alterations, depression and anxiety, and abnormal executive and working memory related functions. On the other hand, insulin-like growth factor 1 (IGF-1) is an endocrine, paracrine and autocrine hormone with several functions including tissue growth and development, insulin-like activity, proliferation, pro-survival, anti-aging, antioxidant and neuroprotection, among others. Herein this review tries to summarize all experimental and clinical data to understand the pathophysiology and development of PD, as well as its clear association with IGF-1, supported by several lines of evidence: (1) IGF-1 decreases with age, while aging is the major risk for PD establishment and development; (2) numerous basic and translational data have appointed direct protective and homeostasis IGF-1 roles in all brain cells; (3) estrogens seem to confer women strong protection to PD via IGF-1; and (4) clinical correlations in PD cohorts have confirmed elevated IGF-1 levels at the onset of the disease, suggesting an ongoing compensatory or "fight-to-injury" mechanism.