ATP production

Aims. Acute consumption of sweeteners has become increasingly common in modern diets. However, emerging research suggests that the impact of sweeteners on the hypothalamus, involved in regulating food intake [CA1] and metabolism, may be deleterious. Several studies have raised concerns about their potential effects on brain cellular metabolism (Kohno D et al.,2016), suggesting a mismatch between detection of false sugar and the energy value actually detected. This study aimed to investigate the dose-dependent impact of sweeteners on these energetic processes. Methods. Using the hypothalamic ce

A growing body of evidence emphasizes that hypometabolism taking place in astrocytes may compromise their physiological neuro-supportive role and activate a set of pathophysiological pathways contributing to the progression of neurodegenerative diseases, including Alzheimer disease (AD) [1]. Here, we explored the potential role of astrocytes in driving a cascade of detrimental effects in the neighboring neurons and investigated a possible approach to limit the injury in both cell types [2]. To this aim, primary rat cortical astrocytes were exposed to glyceraldehyde (GA) to induce a metabolic s

Parvalbumin-positive (PV+) interneurons within the hippocampal system are crucial for maintaining spatial memory functions that are otherwise impaired in neurodegenerative diseases. To maintain such an extensive control, PV+ interneurons require a high energy demand, which requires highly functional mitochondria. Previous studies have shown dysregulations of mitochondria within the hippocampus (HPC) are apparent early on in cases of Alzheimer’s Disease (AD), even preceding the major pathological hallmarks: tau aggregation, amyloid-beta plaques, and impairments in memory. Optogenetic tools have

Parkinson's disease (PD), characterized by the absence of dopamine in the striatum[1], is caused by the death of the substantia nigra pars compacta dopamine (SNcDA) neurons in the mid-brain. The cause of this cell loss is attributed to irreparable damage due to a dysregulation cascade originating from excess cytosolic dopamine[2]. However, it is unresolved if dopamine dysregulation in SNcDA neurons themselves is the cause of PD or if it is a mere symptom. Here, we introduce a theory of specialized non-causal action potentials that serve metabolic homeostasis called `metabolic spikes' which can