Open AccessHigher GABA concentration in the medial prefrontal cortex of Type 2 diabetes patients is associated with episodic memory dysfunction
Author(s) -
Thielen JanWillem,
Gancheva Sofiya,
Hong Donghyun,
Rohani Rankouhi Seyedmorteza,
Chen Bixia,
Apostolopoulou Maria,
AnadolSchmitz Evrim,
Roden Michael,
Norris David G.,
Tendolkar Indira
Publication year - 2019
Publication title -
human brain mapping
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.005
H-Index - 191
eISSN - 1097-0193
pISSN - 1065-9471
DOI - 10.1002/hbm.24702
Subject(s) - prefrontal cortex , precuneus , glutamate receptor , neuroscience , medicine , endocrinology , type 2 diabetes , psychology , diabetes mellitus , functional magnetic resonance imaging , receptor , cognition
Type 2 diabetes (T2D) is associated with an accelerated episodic memory decline, but the underlying pathophysiological mechanisms are not well understood. Hallmarks of T2D comprise impairment of insulin secretion and insulin sensitivity. Insulin signaling modulates cerebral neurotransmitter activity, including the excitatory glutamate and inhibitory gamma‐aminobutyric acid (GABA) systems. Here we tested the hypothesis that the glutamate and GABA systems are altered in T2D patients and this relates to memory decline and insulin resistance. Using 1 H‐magnetic resonance spectroscopy (MRS), we examined glutamate and GABA concentrations in episodic memory relevant brain regions (medial prefrontal cortex and precuneus) of T2D patients and matched controls. Insulin sensitivity was measured by hyperinsulinemic‐euglycemic clamps and memory performance was assessed using a face‐profession associations test. T2D patients exhibited peripheral insulin resistance and had a decreased memory for face‐profession associations as well as elevated GABA concentration in the medial prefrontal cortex but not precuneus. In addition, medial prefrontal cortex GABA concentration was negatively associated with memory performance suggesting that abnormal GABA levels in the medial prefrontal cortex are linked to the episodic memory decline that occurs in T2D patients.