Inflammation in the CNS: Understanding Various Aspects of the Pathogenesis
of Alzheimer's Disease

Doroszkiewicz, Julia; Mroczko, Piotr; Kulczyńska-Przybik, Agnieszka

doi:10.2174/1567205018666211202143935

Cited by 4 publications

(4 citation statements)

References 197 publications

(220 reference statements)

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“… 10 , 106 Airway inflammation is known to provoke neuroinflammation in animal models of asthma, 9 potentially via circumventricular organs, 17 , 106 and there is increasing evidence suggesting that neuroinflammation contributes to neurodegeneration and Alzheimer’s disease pathophysiology. 101 , 103 , 107 In addition to direct effects of airway inflammation on the brain, there are multiple pathways through which asthma may influence brain health. For example, asthma is known to affect the vasculature 108 , 109 and vascular dysfunction contributes to Alzheimer’s disease etiopathogenesis.…”

Section: Discussionmentioning

confidence: 99%

Impact of asthma on the brain: evidence from diffusion MRI, CSF biomarkers and cognitive decline

Nair

Hulle

Bendlin

et al. 2023

Brain Communications

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Chronic systemic inflammation increases the risk of neurodegeneration, but the mechanisms remain unclear. Part of the challenge in reaching a nuanced understanding is the presence of multiple risk factors that interact to potentiate adverse consequences. To address modifiable risk factors and mitigate downstream effects, it is necessary, although difficult, to tease apart the contribution of an individual risk factor by accounting for concurrent factors such as advanced age, cardiovascular risk, and genetic predisposition. Using a case-control design, we investigated the influence of asthma, a highly prevalent chronic inflammatory disease of the airways, on brain health in participants recruited to the Wisconsin Alzheimer’s Disease Research Center (31 asthma patients, 186 non-asthma controls, aged 45–90 years, 62.2% female, 92.2% cognitively unimpaired), a sample enriched for parental history of Alzheimer’s disease. Asthma status was determined using detailed prescription information. We employed multi-shell diffusion weighted imaging scans and the three-compartment neurite orientation dispersion and density imaging model to assess white and gray matter microstructure. We used cerebrospinal fluid biomarkers to examine evidence of Alzheimer’s disease pathology, glial activation, neuroinflammation and neurodegeneration. We evaluated cognitive changes over time using a preclinical Alzheimer cognitive composite. Using permutation analysis of linear models, we examined the moderating influence of asthma on relationships between diffusion imaging metrics, CSF biomarkers, and cognitive decline, controlling for age, sex, and cognitive status. We ran additional models controlling for cardiovascular risk and genetic risk of Alzheimer’s disease, defined as a carrier of at least one apolipoprotein E (APOE) ε4 allele. Relative to controls, greater Alzheimer’s disease pathology (lower amyloid-β42/amyloid-β40, higher phosphorylated-tau-181) and synaptic degeneration (neurogranin) biomarker concentrations were associated with more adverse white matter metrics (e.g., lower neurite density, higher mean diffusivity) in patients with asthma. Higher concentrations of the pleiotropic cytokine IL-6 and the glial marker S100B were associated with more salubrious white matter metrics in asthma, but not in controls. The adverse effects of age on white matter integrity were accelerated in asthma. Finally, we found evidence that in asthma, relative to controls, deterioration in white and gray matter microstructure was associated with accelerated cognitive decline. Taken together, our findings suggest that asthma accelerates white and gray matter microstructural changes associated with aging and increasing neuropathology, that in turn, are associated with more rapid cognitive decline. Effective asthma control, on the other hand, may be protective and slow progression of cognitive symptoms.

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Section: Discussionmentioning

confidence: 99%

Impact of asthma on the brain: evidence from diffusion MRI, CSF biomarkers and cognitive decline

Nair

Hulle

Bendlin

et al. 2023

Brain Communications

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“…According to existing theories, curcumin works primarily by inhibiting NFkB, which is accomplished by preventing IkB phosphorylation and subsequent NFkB activation [ 134 ]. Curcumin can also prevent APP-cleaving enzymes such as B-secretase from functioning (BACE-1) [ 135 , 136 ].…”

Section: Beneficial Foods and Nutrientsmentioning

confidence: 99%

Molecular Aspects of a Diet as a New Pathway in the Prevention and Treatment of Alzheimer’s Disease

Doroszkiewicz

Mroczko

Rutkowski³

et al. 2023

IJMS

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Alzheimer’s disease is the most common cause of dementia in the world. Lack of an established pathology makes it difficult to develop suitable approaches and treatment for the disease. Besides known hallmarks, including amyloid β peptides cumulating in plaques and hyperphosphorylated tau forming NFTs, inflammation also plays an important role, with known connections to the diet. In AD, adhering to reasonable nutrition according to age-related principles is recommended. The diet should be high in neuroprotective foods, such as polyunsaturated fatty acids, antioxidants, and B vitamins. In addition, foods capable of rising BDNF should be considered because of the known profitable results of this molecule in AD. Adhering to beneficial diets might result in improvements in memory, cognition, and biomarkers and might even reduce the risk of developing AD. In this review, we discuss the effects of various diets, foods, and nutrients on brain health and possible connections to Alzheimer’s disease.

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“…The primary mechanism by which curcumin exerts its effects is thought to be through NFkB inhibition, which is achieved by blocking IkB phosphorylation and subsequent NFkB activation [ 91 ]. Moreover, curcumin has the ability to block APP-cleaving enzymes such as β-secretase (BACE-1) [ 92 , 93 ].…”

Section: Alternative Approachmentioning

confidence: 99%

New Possibilities in the Therapeutic Approach to Alzheimer’s Disease

Doroszkiewicz

Mroczko

2022

IJMS

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Despite the fact that Alzheimer’s disease (AD) is the most common cause of dementia, after many years of research regarding this disease, there is no casual treatment. Regardless of the serious public health threat it poses, only five medical treatments for Alzheimer’s disease have been authorized, and they only control symptoms rather than changing the course of the disease. Numerous clinical trials of single-agent therapy did not slow the development of disease or improve symptoms when compared to placebo. Evidence indicates that the pathological alterations linked to AD start many years earlier than a manifestation of the disease. In this pre-clinical period before the neurodegenerative process is established, pharmaceutical therapy might prove invaluable. Although recent findings from the testing of drugs such as aducanumab are encouraging, they should nevertheless be interpreted cautiously. Such medications may be able to delay the onset of dementia, significantly lowering the prevalence of the disease, but are still a long way from having a clinically effective disease-modifying therapy.

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Inflammation in the CNS: Understanding Various Aspects of the Pathogenesis of Alzheimer's Disease

Cited by 4 publications

References 197 publications

Impact of asthma on the brain: evidence from diffusion MRI, CSF biomarkers and cognitive decline

Impact of asthma on the brain: evidence from diffusion MRI, CSF biomarkers and cognitive decline

Molecular Aspects of a Diet as a New Pathway in the Prevention and Treatment of Alzheimer’s Disease

New Possibilities in the Therapeutic Approach to Alzheimer’s Disease

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