Does Inflammation Play a Major Role in the Pathogenesis of Alzheimer's Disease?

Abstract

Alzheimer's disease (AD) is a neurodegenerative disease leading to dementia for which no effective medicine exists. Currently, the goal of therapy is only to slow down the inevitable progression of the disease and reduce some symptoms. AD causes the accumulation of proteins with the pathological structure of Aβ and tau and the induction of inflammation of nerves in the brain, which lead to the death of neurons. The activated microglial cells produce pro-inflammatory cytokines that induce a chronic inflammatory response and mediate synapse damage and the neuronal death. Neuroinflammation has been an often ignored aspect of ongoing AD research. There are more and more scientific papers taking into account the aspect of neuroinflammation in the pathogenesis of AD, although there are no unambiguous results regarding the impact of comorbidities or gender differences. This publication concerns a critical look at the role of inflammation in the progression of AD, based on the results of our own in vitro studies using model cell cultures and other researchers.

The role of Bacillus Calmette-Guérin administration on the risk of dementia in bladder cancer patients: a systematic review and meta-analysis

“…The pathogenesis of AD includes two key features: accumulation of amyloid β (Aβ) plaques and neurofibrillary tangles (hyperphosphorylated tau protein) (Kinney et al, 2018 ). Aβ and tau species could activate astrocytes and the brain's resident macrophages (microglia), which release many pro-inflammatory cytokines, such as tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β), and oxidative stress biomarkers (Singh et al, 2019a ; Novoa et al, 2022 ; Wiatrak et al, 2022 ). Then, neuroinflammation is triggered.…”

“…Then, neuroinflammation is triggered. However, this inflammatory response can lead to Aβ and tau overproduction and induce neurodegeneration, synapse damage, and neuronal death (Novoa et al, 2022 ; Wiatrak et al, 2022 ). In general, accumulating evidence supports that the development of AD is associated with the immune system.…”

A bibliometric review on vitamins and Alzheimer’s disease between 1996 and 2023

“…The mechanism of AD development has not been fully elucidated, although both genetic and environmental factors are involved (Cummings et al, 2022). The two hallmarks of AD are the extracellular deposits of neurotoxic β-amyloid (Aβ) in the brain and the accumulation of tau protein tangles in neurons, which lead to neuronal cell loss and damage to the vascular system, causing reduced blood flow to the brain and consequential cognitive impairment (Lei et al, 2021;Gabarro-Solanas and Urban, 2023;Wiatrak et al, 2023). Above all, oxidative stress has received considerable attention over the past several decades given its possible role in neurodegenerative processes (Chikara et al, 2018;Bai et al, 2022).…”