Neuroplasticity Improves Bipolar Disorder: A Review

Abstract

Bipolar disorder (BD) is known for impairments in neurotrophic and neuroprotective processes, which translate into emotional and cognitive deficits affecting various brain regions. Using its neuroplastic properties, lithium, thus far, is the mood stabilizer used to amend the pathophysiological imbalance in BD. Neuroplasticity has gained massive popularity in the research department in the past decade, yet it lacks direct effort in changing the protocol through which physicians treat BD. Physical activity alongside cognitive therapy is theorized to produce long-term changes in the executive control network due to the assimilation of new neurons, amendment of emotional lability through hippocampal neurogenesis, and strengthening the stability of frontosubcortical and prefrontolimbic brain regions via neurogenesis. This review aims to provide an incentive for utilizing neuroplastic mechanisms concerning impairments dispensed by BD.

Nutritional interventions for the prevention and treatment of neurological disorders such as anxiety, bipolar disorder, depression, epilepsy, multiple sclerosis, and schizophrenia

“…The former is diagnosed in patients who have had at least one manic episode, marked by heightened activity and grandiosity, after which they experience a depressive or hypomanic episode [104][105][106][107]. In contrast, BD-II involves hypomanic and depressive episodes without manic episodes [108,109]. Some patients with BD display progressive alterations in neuroanatomy such as decreasing cortical thickness, lateral ventricle enlargement, or decreasing hippocampal volume, which is correlated with BD progression [110][111][112][113][114].…”

“…Ultimately, BD is a complex illness in luenced by a variety of genetic, environmental, and social factors with a pathophysiology including disrupted brain development; altered chronobiology and neuroplasticity; mitochondrial dysfunction; oxidative and nitrosative stress; endoplasmic reticulum stress; and defects in signaling involving apoptosis, neurotrophic factors, in lammation, calcium and neurotransmitters [115][116][117][118][119][120][121][122]. The parietal lobewhich plays an important role in memory, attention, and other cognitive functions-is also involved in BD development [109,123].…”

Common and Specific Intrinsic Functional Network Related to Episode Dynamics during Treatment in Bipolar Spectrum

“…This aligns with decreased neurotransmitter, such as dopamine[9] and glutamate[6], emphasizing the important role of these specific brain regions in the pathogenesis of depressive disorders. In rBD patients, from the perspective of neuroplasticity and adaptability, these findings may indicate neuroplastic changes in these regions [15], where treatment could lead to the reorganization of neuronal connections to adapt to new environments or situations, potentially correlating with symptom relief in patients. Lastly, the nodal degree of common lesioned brain areas negatively correlates with the degree of cognitive impairment, highlighting the significant impact of these regions on emotion regulation and cognitive function in bipolar disorder patients.…”

Role of microtubule actin crosslinking factor 1 (MACF1) in bipolar disorder pathophysiology and potential in lithium therapeutic mechanism

“…BPAD is associated with decreased dendrite length, density, and branching—all of which are significant to proper plasticity of synapses [ 82 , 83 ]. Indeed, BPAD is associated with altered structural plasticity of these dendritic spines and BPAD has been associated with altered excitatory/inhibitory synapse ratios [ 82 , 84 , 85 ]. All these mechanisms point toward another hypothesis in BPAD etiology: altered morphological function in dendritic spines and axons.…”