Can Control Infections Slow Down the Progression of Alzheimer’s Disease? Talking About the Role of Infections in Alzheimer’s Disease

Abstract

Alzheimer’s disease as the most common age-related dementia affects more than 40 million people in the world, representing a global public health priority. However, the pathogenesis of Alzheimer’s disease (AD) is complex, and it remains unclear. Over the past decades, all efforts made in the treatments of AD, with targeting the pathogenic amyloid β (Aβ), neurofibrillary tangles, and misfolded tau protein, were failed. Recently, many studies have hinted that infection, and chronic inflammation that caused by infection are crucial risk factors for AD development and progress. In the review, we analyzed the role of infections caused by bacteria, viruses, and other pathogens in the pathogenesis of AD and its animal models, and explored the therapeutic possibility with anti-infections for AD. However, based on the published data, it is still difficult to determine their causal relationship between infection and AD due to contradictory results. We think that the role of infection in the pathogenesis of AD should not be ignored, even though infection does not necessarily cause AD, it may act as an accelerator in AD at least. It is essential to conduct the longitudinal studies and randomized controlled trials in humans, which can determine the role of infection in AD and clarify the links between infection and the pathological features of AD. Finding targeting infection drugs and identifying the time window for applying antibacterial or antiviral intervention may be more promising for future clinical therapeutic strategies in AD.

Recent insights into viral infections as a trigger and accelerator in alzheimer's disease

“… 1 It is the most common form of dementia, affecting >50 million people today worldwide and this number is set to increase in the coming decades. [2] , [3] Patients are characterized by progressive and disabling deficits in cognitive function, ultimately leading to impairment in daily life quality. 4 Pathologically, AD brains are marked by the deposition of amyloid-beta (Aβ) protein in senile plaques outside neurons and the formation of neurofibrillary tangles (NFT) composed of hyperphosphorylated Tau (p-Tau) protein inside neurons.…”

New Insights into the Molecular Interplay between Human Herpesviruses and Alzheimer’s Disease—A Narrative Review

“…Although the mechanisms related to the disease pathology have been under substantial investigation and several hypotheses have been proposed, there is no accepted theory at the moment for explaining AD pathogenesis [ 2 , 9 ]. Emerging evidence in recent years supports that a wide spectrum of infectious agents (viruses, bacteria, fungi, and protozoa) can cross the blood–brain barrier (BBB) and might play a triggering role in AD development [ 11 , 12 , 13 ]. Among them, herpesviruses represent the most studied family of neurotropic pathogens [ 14 ].…”

“…Apart from HHVs, other neurotropic viruses are reported to have an impact on cognitive decline within the context of AD, including the human immunodeficiency virus (HIV), the human T cell leukemia virus type I (HTLV-1), the influenza virus, and the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) [ 11 , 12 , 46 ]. Moreover, current findings support that patients with chronic hepatitis C virus (HCV) infection appear to exhibit cognitive impairment and that it may increase the risk for dementia [ 47 , 48 , 49 ].…”

Circadian dysregulation and Alzheimer’s disease: A comprehensive review

“…As of now (2022) the scientific community only has a cursory understanding of the many benefits attributed to a good night’s rest. It seems apparent that memory consolidation and the pruning of excess neurons (elimination of cortical matter that is, in effect, “dead weight”) are drastically upregulated during sleep, and the immunal and bodily recovery benefits of sleep have been well documented [18, 19]. However, given the observed restorative effect that sufficient sleep can have on the human body and mind, it is entirely likely that these findings only scratch the surface of the benefits accrued with optimized sleep patterns over time.…”

“…Studies have shown that late onset depression can presage MCI symptoms, with older populations being significantly more likely to exhibit dementia-like behaviors within five years of depression onset [194]. Moreover, there is a noteworthy correlation between the preclinical deposition of the Aβ peptide, and depressive symptoms, with heightened Aβ deposition making an individual four times more likely to develop depressive symptoms [18].…”