Episodic memory (EM) alterations are a hallmark of Alzheimer's disease (AD). We assessed EM longitudinally in cognitively normal elders at-risk for AD (with subjective memory complaints), as a function of amyloid-β (Aβ) burden, neurodegeneration (N), and progression to prodromal AD. We stratified 264 INSIGHT-preAD study subjects in controls (Aβ-/N-), stable/N- or N + (Aβ +), and progressors/N- or N + (Aβ +) groups (progressors were included only until AD-diagnosis).
View Article and Find Full Text PDFIntroduction: Anticipating the diagnosis of Alzheimer's disease (AD) at an early asymptomatic at-risk stage, where therapeutics can more effectively delay conscious cognitive decline, is currently among the biggest challenges in the field. Herein, we aimed to compare the capacity of the Memory Binding Test (MBT) with the official diagnostic tool, the Free and Cued Selective Reminding Test (FCSRT), to anticipate AD diagnosis at an early preclinical stage based on the associative memory component of MBT (binding), suggested as more sensitive to the emergence of subtle episodic memory (EM) deficits (AD hallmark).
Methods: We assessed the tests performance longitudinally (over 5 years) in 263 cognitively-normal elderly individuals at risk of AD (>6 months of subjective memory complaints) using linear mixed-effect models controlled for age, sex, and education.
Unawareness of memory deficits is an early manifestation in patients with Alzheimer's disease (AD), which often delays diagnosis. This intriguing behavior constitutes a form of anosognosia, whose neural mechanisms remain largely unknown. We hypothesized that anosognosia may depend on a critical synaptic failure in the error-monitoring system, which would prevent AD patients from being aware of their own memory impairment.
View Article and Find Full Text PDFGamma hydroxybutyric acid (GHB) has been used recreationally for nearly three decades and its chronic use is frequently associated with serious adverse events including GHB-intoxication with GHB-induced comas. Moreover, despite its low prevalence, the number of individuals with GHB-use disorders is steadily increasing. However, the risk-factors associated with chronic GHB-use or the development of a GHB-use disorders remain poorly understood.
View Article and Find Full Text PDFBackground And Aims: The regular use of gamma-hydroxybutyrate acid (GHB) can induce GHB-induced comas. Other substance use disorders are associated with alterations in brain structure and impulsivity. Here we aim to investigate if these are also modulated by either regular GHB use or GHB-induced comas.
View Article and Find Full Text PDFBackground: Gamma-hydroxybutyric acid (GHB) is a drug of abuse associated with increased emergency room attendances, due to GHB-induced comas. Withdrawal from GHB often increases social anxiety and is linked to alterations in emotion processing. However, little is known about the effects of GHB-use and GHB-induced comas on affect regulation in humans.
View Article and Find Full Text PDFGamma-hydroxybutyrate acid (GHB) is a recreational drug with a high addictive potential. Severe side effects such as GHB-induced coma are common and linked to increased emergency room attendances. Task-based functional-imaging studies have revealed an association between the regular use of GHB and multiple GHB-induced comas, and altered neurocognitive function.
View Article and Find Full Text PDFBackground: Gamma-hydroxybutyric acid (GHB) is a recreational drug associated with increasing numbers of GHB-dependent patients and emergency attendances often related to GHB-induced comas. Working memory (WM) deficits have been reported in association with GHB use, and animal studies have shown that GHB induces oxidative stress in vulnerable WM-related brain areas such as the dorsolateral prefrontal cortex (DLPFC). However, the effects of chronic GHB use and multiple GHB-induced comas on WM-related brain function in humans remains unknown.
View Article and Find Full Text PDFBackground: Gamma-Hydroxybutyric acid (GHB) is a drug of abuse associated with increasing numbers of GHB-dependent patients and emergency attendances often related to GHB-induced coma. Animal studies suggest that GHB induces oxidative stress in the hippocampus, resulting in memory impairments. However, the consequences of chronic GHB use and GHB-induced coma on human brain function and cognition are unknown.
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