Researchers measured inflammation in more than 12,000 middle-aged adults. They then assessed the cognitive function of the participants in three separate visits over the next 20 years. They found that after adjusting for demographic and other variables, inflammation appeared to be associated with increased cognitive decline. People in the study who had higher inflammation scores experienced 7.8% greater cognitive decline when compared with study participants who had lower scores.
Chronic activation of the brain’s immune cells, called “glial cells,” increases with age, elevating production of beta-amyloid and tau proteins, the hallmarks of Alzheimer’s disease. Independently, sleep disturbance has been linked to Alzheimer’s disease pathology in the brain, and studies have also indicated an association between sleep disturbance and inflammation.The link between brain inflammation and sleep disturbance was shown by 58 cognitively unimpaired adults in their 50s and 60s. Activation of two types of glial cells — microglia and astrocytes, which trigger brain inflammation — was associated with disrupted expression of fast sleep spindles.
Brain inflammation (neuroinflammation) has a downstream effect on Alzheimer’s disease-related tau proteins and neuronal synaptic integrity. This results in deficits in the brain’s capacity to generate fast sleep spindles, which contribute to age-related memory impairment in older adults. An inflammatory response to environmental risk factors may be, directly or indirectly, modulated by genetic variation, and may represent a significant component or driver of neurodegenerative disease.
Chronic inflammation can inhibit hippocampal neurogenesis.
Converging animal and human evidence suggests that inflammation is a shared mechanism, contributing to both cognitive decline and abnormalities in brain structure and metabolism.
Provoking inflammation in mice led to persistent changes in gene expression in brain microglia — even though the molecules themselves didn’t enter their brains.
The importance of minimizing chronic inflammation was shown by a study of 47 young and 46 older generally healthy adults.
The importance of minimizing chronic inflammation was shown by a study of 12,336 people with an average age of 57 for 20 years.
The importance of minimizing chronic inflammation was shown by a study of 1588 people with mean age of 69 years.
Chronic inflammation damages white matter in the ageing brain
An inflammation inhibitor blocks neurodevelopmental disorders in mouse model.
Chronic inflammation injures via PGE2, as demonstrated in aged mice.
Old genetically modified mice with the EP2 receptor (that senses inflammation) removed learned and remembered just as well as their young counterparts.
Brain inflammation is emerging as a contributor to the development of Alzheimer’s disease, and that inflammation is driven by non-neuronal cells in the brain, including astrocytes. Suppressing the inflamed astrocytic state halts disease progression.
Even transient inflammation is to be avoided
How to avoid chronic inflammation
Low levels of bacterially derived short-chain fatty acids (SCFAs) in the aged microbiota are partially to blame gut microbiom-caused inflammation. This is caused, in part, by a low-solutble fiber diet. The continuous presence of cytokines (in indicator of inflammation) appears sufficient to inflict neuronal damage and ultimately forms the basis for age-related neurodegeneration. This is especially important for those genetically at risk for Alzheimer’s.
Sleep loss exerts a strong regulatory influence on peripheral levels of inflammatory mediators of the immune response. An increasing number of research projects support the existence of reciprocal regulation between sleep and low-intensity inflammatory response. Recent studies show that sleep deficient humans and rodents exhibit a proinflammatory component
For those on the autistic spectrum, brain inflammation is likely. Avoiding brain inflammation may be especially important for all. Neuroinflammation is the key driver of the spread of pathologically misfolded proteins in the brain and causes cognitive impairment in patients with Alzheimer’s disease. Inflammation in the CNS increases in normal aging and is intimately related to markers of neurodegeneration in the preclinical stages of AD. An inflammatory feedback loop contributes to neurodegeneration/several forms of dementia.
Targeting brain inflammation:
Catechins from green tea
A robust circadian oscillation
Exactly how curcumin prevents cognitive decline is not certain, but it may be due to its ability to reduce brain inﬂammation.
In vitro studies, curcumin has been reported to inhibit amyloid-β-protein (Aβ) aggregation, and Aβ-induced inflammation.
Curcumin could be a potential therapeutic agent for the treatment of neurodegenerative disorders via suppressing neuroinflammatory responses.
Due to various effects of curcumin, such as decreased Beta-amyloid plaques, delayed degradation of neurons, metal-chelation, anti-inflammatory, antioxidant and decreased microglia formation, the overall memory in patients with AD has improved.
Treatment of microglial cells with curcumin decreased inflammation. Curcumin, able to enter brain tissue in biologically relevant concentrations, reduced acute and transient microglia activation, pro-inflammatory mediator production, and the behavioral symptoms of sickness.
Curcumin re-establishes antioxidant enzyme activity to reduce neuroinflammation, moderates the amyloidogenic pathway peripherally and centrally by binding with amyloid β (Aβ) to render it nontoxic.
Chronic inflammation spreads to the nervous system/brain. Curcumin dampens chronic inflammation.
Curcumin powerfully inhibits neuroinflammation in mice and rats.
People with longer periods of untreated depression, lasting more than a decade, had significantly more brain inflammation compared to those who had less than 10 years of untreated depression.
Oxidation of arachidonic acid (AA) (found in meat) produces pro-inflammatory prostaglandins, leukotrienes, and thromboxanes. One of the lyso-glycerophospholipids, the other products of reactions catalyzed by phospholipase A2, is used for the synthesis of pro-inflammatory platelet-activating factor. These pro-inflammatory mediators intensify. neuroinflammation.
When lithium reaches the brain, it both reduces levels of the inflammatory compound arachidonic acid and increases levels of the anti-inflammatory compound 17-OH-DHA, which is formed from an omega-3 fatty acid—docosahexaenoic acid. Low-dose lithium (5 mg) is available as a nutritional supplement.
Avoid a high–fat (fast food) diet, as well as arachidonic acid (from meat). Consumption of a high-fat diet — specifically diets that include high amounts of fats and carbohydrates — stimulates hypothalamic inflammation as early as three days after consumption of a high-fat diet, even before the body begins to display signs of obesity.
The AD-stimulating pathway begins inside of us—in our GI-tract microbiome—and therefore is very “locally sourced” and active throughout our lives. The highly potent neurotoxin Bacteroides fragilis – lipopolysaccharide (BF-LPS) is a natural by-product of GI-tract-based microbial metabolism. Bacteroides fragilis abundance in the microbiome, which is the source of the neurotoxin BF-LPS, can be regulated by dietary fiber intake.
Genetic data of 294 ,970 participants in the UK Biobank, using Mendelian randomization to show the association between vitamin D and C-reactive protein levels, an indicator of inflammation.
Docosahexaenoic acid (DHA) and its lipid mediators prevent neuroinflammation by inhibiting transcription factor NFkappaB, preventing cytokine secretion, blocking the synthesis of prostaglandins, leukotrienes, and thromboxanes, and modulating leukocyte trafficking.
Diet-induced accumulation of DHA in the brain protects against postischemic inflammation and injury.
The other major n-3 PUFA, eicosapentaenoic acid, showed similar effects of DHA on inflammation and HO-1 in repeated key experiments.
Enriched environment vs. brain inflammation (in mice)
EPA – another component of fish oil
Exercise vs. glial inflammation.
Avoid head injury – wear a helmet
Dietary luteolin enhanced spatial working memory by mitigating microglial-associated inflammation in the hippocampus. Luteolin is found in rosemary, radicchio, celery, thyme, green peppers, cabbage, chamomile, and other foods.
An 8-week Mindfulness-Based Stress Reduction (MBSR) intervention successfully reduced the stress response to using topical application of capsaicin cream to forearm skin.
Mindfulness meditation training functionally couples the default mode network (DMN) with a region known to be important in top-down executive control at rest, which, in turn, is associated with improvements in a marker of inflammatory disease risk.
Olive oil reduces brain inflammation but most importantly activates a process known as autophagy,
Mice treated with PQQ demonstrated marked attenuation of neuroinflammation. PQQ protected primary cortical neurons against microglia-mediated neurotoxicity.
PQQ alters indicators of inflammation and mitochondrial-related metabolism in human subjects.
Rutin, a biologically active flavonoid, protects the rat brain against several insults through its antioxidant and anti-inflammatory properties.
When applied to a mouse model of tauopathy, rutin reduced pathological tau levels, regulated tau hyperphosphorylation, suppressed gliosis and neuroinflammation by downregulating NF-kB pathway, prevented microglial synapse engulfment, and rescued synapse loss in mouse brains, resulting in a significant improvement of cognition. Here are dietary sources of rutin.
The phytoestrogen quercetin and the lignan sesamin may be regarded as potent, natural, anti-inflammatory compounds. reduces neuroinflammation.
Sulforaphane enhances endogenous the anti-inflammatory system, reduces neuroinflammation in the rat hippocampus.
The inhibition of inflammatory response with sulforaphane treatment improves outcomes in rats after focal cerebral ischemia.
Avoid excessive sugar and simple carbs