Healthy lifestyles and wellbeing reduce neuroinflammation and prevent neurodegenerative and psychiatric disorders

Abstract

Since the mid-20th century, Western societies have considered productivity and economic outcomes are more important than focusing on people's health and wellbeing. This focus has created lifestyles with high stress levels, associated with overconsumption of unhealthy foods and little exercise, which negatively affect people's lives, and subsequently lead to the development of pathologies, including neurodegenerative and psychiatric disorders. Prioritizing a healthy lifestyle to maintain wellbeing may slow the onset or reduce the severity of pathologies. It is a win-win for everyone; for societies and for individuals. A balanced lifestyle is increasingly being adopted globally, with many doctors encouraging meditation and prescribing non-pharmaceutical interventions to treat depression. In psychiatric and neurodegenerative disorders, the inflammatory response system of the brain (neuroinflammation) is activated. Many risks factors are now known to be linked to neuroinflammation such as stress, pollution, and a high saturated and trans fat diet. On the other hand, many studies have linked healthy habits and anti-inflammatory products with lower levels of neuroinflammation and a reduced risk of neurodegenerative and psychiatric disorders. Sharing risk and protective factors is critical so that individuals can make informed choices that promote positive aging throughout their lifespan. Most strategies to manage neurodegenerative diseases are palliative because neurodegeneration has been progressing silently for decades before symptoms appear. Here, we focus on preventing neurodegenerative diseases by adopting an integrated "healthy" lifestyle approach. This review summarizes the role of neuroinflammation on risk and protective factors of neurodegenerative and psychiatric disorders.

Keywords: healthy lifestyle; neurodegeneration; neuroinflammation; psychiatric; reduce risk; wellbeing.

FIGURE 1

Selective sites of neuronal death in some neurodegenerative diseases. Pyramidal neurons in the entorhinal cortex layer II and hippocampus layer CA1 in Alzheimer’s disease (AD), dopaminergic neurons in the substantia nigra pars compacta in Parkinson’s disease (PD), GABAergic spiny projection and cholinergic neurons in the striatum, and pyramidal neurons in the cortex in Huntington’s disease (HD), and motor neurons in the motor cortex, brainstem or spinal cord in amyotrophic lateral sclerosis (ALS).

FIGURE 2

A schematic diagram showing the bidirectional communication between central and systemic immune system responses that cause neuroinflammation. Resident immune cells in the brain, microglia and astrocytes, act as scavengers to rapidly react to a pathological event. Immune cells in the periphery communicate with microglia and astrocytes through cytokines and chemokines. Foreign/pathological substances or antigens are drained from the CNS to peripheral lymph nodes where they are processed and presented to adaptive cells by antigen presenting cells. Peripheral innate and adaptive cells react to these signals and antigen presentation and cross the blood brain barrier to help eliminate the pathological event. They are also responsible of neuronal damage by inducing neuroinflammation. APC, antigen-presenting cell; ATP, adenosine triphosphate; CD4 T cell, lymphocyte T helper expressing CD4 (cluster of differentiation 4) glycoprotein; CD8 T cell, cytotoxic T cell expressing CD8; COX-2, cyclooxygenase-2; CXCL10, C-X-C motif chemokine ligand 10; DC, dendritic cell; IL, interleukin; iNOS, inducible nitric oxide synthase; Mϕ, macrophage; MMP3, matrix metalloproteinase-3; Nϕ, neutrophil; NK, natural killer; Th cell, lymphocyte T helper; TNF, tumor necrosis factor.

FIGURE 3

Neuroinflammation is a hallmark of neurodegenerative and psychiatric disorders. Neuroinflammation was identified by positron emission tomography (PET) scans in patients. Presence of activated microglia (colored cells) in: Huntington’s disease (Lois et al., 2018); Parkinson’s disease (Gerhard et al., 2006); multiple sclerosis (Datta et al., 2017); amyotrophic lateral sclerosis (Alshikho et al., 2018); Alzheimer’s disease (Cagnin et al., 2007; Valotassiou et al., 2018); depression (Setiawan et al., 2015), schizophrenia (Doorduin et al., 2009; Marques et al., 2017); and bipolar disorder (Haarman et al., 2014).

FIGURE 4

Risk and protective factors for neuroinflammation and their contributions to positive aging or the development of neurodegenerative and psychiatric disorders.