Inflammation: the link between comorbidities, genetics, and Alzheimer’s disease

Abstract

Alzheimer’s disease (AD) is a neurodegenerative disorder, most cases of which lack a clear causative event. This has made the disease difficult to characterize and, thus, diagnose. Although some cases are genetically linked, there are many diseases and lifestyle factors that can lead to an increased risk of developing AD, including traumatic brain injury, diabetes, hypertension, obesity, and other metabolic syndromes, in addition to aging. Identifying common factors and trends between these conditions could enhance our understanding of AD and lead to the development of more effective treatments. Although the immune system is one of the body’s key defense mechanisms, chronic inflammation has been increasingly linked with several age-related diseases. Moreover, it is now well accepted that chronic inflammation has an important role in the onset and progression of AD. In this review, the different inflammatory signals associated with AD and its risk factors will be outlined to demonstrate how chronic inflammation may be influencing individual susceptibility to AD. Our goal is to bring attention to potential shared signals presented by the immune system during different conditions that could lead to the development of successful treatments.

Neutralization of IL‐17 rescues amyloid‐β‐induced neuroinflammation and memory impairment

“…AD is the most common and most studied neurodegenerative disorder. It has become a critical issue to human health, especially in ageing societies, and therefore, it is a focus of research in the global scientific community (Newcombe et al, 2018). It is a multifactorial disorder primarily characterized by the deposition of amyloid plaques in the brain, leading to irreversible cognitive impairment and neuroinflammation that mainly involves hippocampus and cortex districts Iba-1, S100B, and MPO, and by the inhibition of typical proinflammatory cyto-chemokines in total brain and, more specifically, in the hippocampal and prefrontal cortex regions.…”

Diet Associated with Inflammation and Alzheimer’s Disease

“…The inflammatory events throughout an individual's lifetime suggest the presence of a chronic inflammatory condition. The cumulative effects of this chronic inflammation may impact the different stages of AD [132]. Developing anti-inflammatory approaches to lifestyle habits may likely slow the progression, or delay the onset of AD.…”

“…As the literature indicates, inflammation contributes to AD pathogenesis. Inflammatory pathways can accelerate the progression of AD [131] and several other age-related diseases [132]. An antiinflammatory therapy should be beneficial in delaying the progression of AD.…”

“…It is important to know chronic inflammation is linked to the neurobiology and progression of AD [133] through different mechanisms, such as production and clearance of A␤. A␤ plaques can trigger inflammation in a positive feedback loop [132].…”

Interleukinų IL1A ir IL6 genų polimorfizmas: sąsajų su APOE genotipu ir sporadinės Alzheimerio ligos klinikine eiga paieška

“…Taip pat bu vo nu sta ty tos di des nës IL6 kon cen tra ci jos sergan èiø jø AL sme ge nø skys ty je ir krau jy je [2]. Dau gë ja árody mø, kad uþ de gi mo me dia to riø ge nø po li mor fiz mas, raið ka ir tar pu sa vio sà vei ka taip pat le mia ci to ki nø funk cijas, yra su si ju sios su skir tin ga ri zi ka sirg ti AL [12,33,34]. Anks tes nia me ty ri me bu vo me nu sta tae, kad in ter leu kinø IL1A -889C>T ir IL6 -174G>C ge no ti pai bu vo pa na ðiai pa si skirs tae tarp ser gan èiø jø AL ir kon tro li nës gru pës ti riamø jø [35].…”