The interaction between insulin resistance and Alzheimer's disease: a review article.
Postgrad Med
; 136(4): 377-395, 2024 May.
Article
en En
| MEDLINE
| ID: mdl-38804907
ABSTRACT
Insulin serves multiple functions as a growth-promoting hormone in peripheral tissues. It manages glucose metabolism by promoting glucose uptake into cells and curbing the production of glucose in the liver. Beyond this, insulin fosters cell growth, drives differentiation, aids protein synthesis, and deters degradative processes like glycolysis, lipolysis, and proteolysis. Receptors for insulin and insulin-like growth factor-1 are widely expressed in the central nervous system. Their widespread presence in the brain underscores the varied and critical functions of insulin signaling there. Insulin aids in bolstering cognition, promoting neuron extension, adjusting the release and absorption of catecholamines, and controlling the expression and positioning of gamma-aminobutyric acid (GABA). Importantly, insulin can effortlessly traverse the blood-brain barrier. Furthermore, insulin resistance (IR)-induced alterations in insulin signaling might hasten brain aging, impacting its plasticity and potentially leading to neurodegeneration. Two primary pathways are responsible for insulin signal transmission the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) pathway, which oversees metabolic responses, and the mitogen-activated protein kinase (MAPK) pathway, which guides cell growth, survival, and gene transcription. This review aimed to explore the potential shared metabolic traits between Alzheimer's disease (AD) and IR disorders. It delves into the relationship between AD and IR disorders, their overlapping genetic markers, and shared metabolic indicators. Additionally, it addresses existing therapeutic interventions targeting these intersecting pathways.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Resistencia a la Insulina
/
Transducción de Señal
/
Enfermedad de Alzheimer
/
Insulina
Límite:
Humans
Idioma:
En
Revista:
Postgrad Med
Año:
2024
Tipo del documento:
Article
País de afiliación:
Arabia Saudita