More than Addiction—The Nucleus Accumbens Contribution to Development of Mental Disorders and Neurodegenerative Diseases

Abstract

Stress and negative emotions evoked by social relationships and working conditions, frequently accompanied by the consumption of addictive substances, and metabolic and/or genetic predispositions, negatively affect brain function. One of the affected structures is nucleus accumbens (NAc). Although its function is commonly known to be associated with brain reword responses and addiction, a growing body of evidence also suggests its role in some mental disorders, such as depression and schizophrenia, as well as neurodegenerative diseases, such as Alzheimer’s, Huntington’s, and Parkinson’s. This may result from disintegration of the extensive connections based on numerous neurotransmitter systems, as well as impairment of some neuroplasticity mechanisms in the NAc. The consequences of NAc lesions are both morphological and functional. They include changes in the NAc’s volume, cell number, modifications of the neuronal dendritic tree and dendritic spines, and changes in the number of synapses. Alterations in the synaptic plasticity affect the efficiency of synaptic transmission. Modification of the number and structure of the receptors affects signaling pathways, the content of neuromodulators (e.g., BDNF) and transcription factors (e.g., pCREB, DeltaFosB, NFκB), and gene expression. Interestingly, changes in the NAc often have a different character and intensity compared to the changes observed in the other parts of the basal ganglia, in particular the dorsal striatum. In this review, we highlight the role of the NAc in various pathological processes in the context of its structural and functional damage, impaired connections with the other brain areas cooperating within functional systems, and progression of the pathological processes.

Escaping negative moods and concentration problems play bridge roles in the symptom network of problematic smartphone use and depression

“…These findings are in accordance with the notion that mental dysfunction may be a cause of comorbidity of addiction and depression (46,47). As previous studies have found, addiction and depression have similar manifestations of brain dysfunction (48). Our findings would inspire future research to explore whether depression and PSU have a common neuropsychological basis.…”

Potential therapeutic mechanism of deep brain stimulation of the nucleus accumbens in obsessive-compulsive disorder

“…The nucleus accumbens (NAc) is considered as the limbic-motor interface and plays an important role in brain networks related to motivation and reward processing (Groenewegen et al, 1996;Salamone et al, 2007;Nicola, 2010;Floresco, 2015). It has been suggested that dysfunction of the NAc is associated with various neuropsychiatric disorders (Mavridis, 2015;Park et al, 2019;Gendelis et al, 2021;Bayassi-Jakowicka et al, 2022). The NAc is one of the most commonly used neurosurgical targets in the treatment of OCD (Denys et al, 2010;Greenberg et al, 2010;Huys et al, 2019;Raviv et al, 2020), however, there are still many questions related to the use of DBS of the NAc (NAc-DBS) for the treatment of OCD, because the relevant underlying pathophysiological mechanisms are unclear, including the effect of NAc-DBS on neural electrophysiological activities and neurotransmitters activities.…”

Altered functional connectivity of nucleus accumbens subregions associates with non‐motor symptoms in Parkinson's disease

“…The DMN is mainly composed of the medial prefrontal cortex, posterior cingulate cortex/precuneus, and lateral parietal cortex, 10 which involves social behavior, mood control, and motivational drive. Hyperconnection between the ventral subiculum (BA36) and NAc involves in the development of schizophrenia, and disconnections between the ventral tegmental area, NAc, and hippocampus (BA36) were recorded in Alzheimer's disease 11 …”

“…Hyperconnection between the ventral subiculum (BA36) and NAc involves in the development of schizophrenia, and disconnections between the ventral tegmental area, NAc, and hippocampus (BA36) were recorded in Alzheimer's disease. 11 …”

“…Hyperconnection between the ventral subiculum (BA36) and NAc involves in the development of schizophrenia, and disconnections between the ventral tegmental area, NAc, and hippocampus (BA36) were recorded in Alzheimer's disease. 11 The role of NAc in the NMS of PD has received attention in recent years. Compared with healthy controls, the volume of NAc is significantly decreased in PD patients with mild cognitive impairment 12 or with apathy.…”