Organization of Inflammatory Processes in Alzheimer’s Disease

2000 ◽  
pp. 1-7
Author(s):  
J. Rogers ◽  
Y. Shen
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Inflammatory Processes

scholarly journals Fingolimod Rescues Memory and Improves Pathological Hallmarks in the 3xTg-AD Model of Alzheimer’s Disease

2022 ◽  
Author(s):  
Steven G. Fagan ◽  
Sibylle Bechet ◽  
Kumlesh K. Dev
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Biochemical Analysis ◽  
Spatial Working Memory ◽  
Cell Number ◽  
Model Of Alzheimer’S Disease ◽  
Candidate Drug ◽  
Inflammatory Processes ◽  
The Brain ◽  
Ad Mouse Model

AbstractTherapeutic strategies for Alzheimer’s disease (AD) have largely focused on the regulation of amyloid pathology while those targeting tau pathology, and inflammatory mechanisms are less explored. In this regard, drugs with multimodal and concurrent targeting of Aβ, tau, and inflammatory processes may offer advantages. Here, we investigate one such candidate drug in the triple transgenic 3xTg-AD mouse model of AD, namely the disease-modifying oral neuroimmunomodulatory therapeutic used in patients with multiple sclerosis, called fingolimod. In this study, administration of fingolimod was initiated after behavioral symptoms are known to emerge, at 6 months of age. Treatment continued to 12 months when behavioral tests were performed and thereafter histological and biochemical analysis was conducted on postmortem tissue. The results demonstrate that fingolimod reverses deficits in spatial working memory at 8 and 12 months of age as measured by novel object location and Morris water maze tests. Inflammation in the brain is alleviated as demonstrated by reduced Iba1-positive and CD3-positive cell number, less ramified microglial morphology, and improved cytokine profile. Finally, treatment with fingolimod was shown to reduce phosphorylated tau and APP levels in the hippocampus and cortex. These results highlight the potential of fingolimod as a multimodal therapeutic for the treatment of AD.

scholarly journals Astrocytes and Inflammatory Processes in Alzheimer’s Disease

2020 ◽  
Author(s):  
Soraya L. Valles ◽  
Federico Burguet ◽  
Antonio Iradi ◽  
Martin Aldasoro ◽  
Jose M. Vila ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Inflammatory Processes

Inflammatory processes and Alzheimer’s disease

2004 ◽  
Vol 4 (5) ◽  
pp. 793-798 ◽  
Author(s):  
Sally Walsh ◽  
Paul S Aisen
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Inflammatory Processes

P4-340 Immunological assessment of acute CNS inflammatory processes elicited in an Alzheimer's disease mouse model following HSV amplicon-based Aβ vaccination

2004 ◽  
Vol 25 ◽  
pp. S572
Author(s):  
William J. Bowers ◽  
Michael A. Mastrangelo ◽  
Hilary A. Stanley ◽  
Ya-Hui Chiu ◽  
Howard J. Federoff
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Model Following ◽  
Inflammatory Processes

scholarly journals The Impact of Systemic Inflammation on Alzheimer’s Disease Pathology

2022 ◽  
Vol 12 ◽  
Author(s):  
Junhua Xie ◽  
Lien Van Hoecke ◽  
Roosmarijn E. Vandenbroucke
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Rational Design ◽  
Neurodegenerative Disorder ◽  
Peripheral Inflammation ◽  
Comprehensive Overview ◽  
Age Related ◽  
Symptomatic Medication ◽  
Inflammatory Processes ◽  
The Impact

Alzheimer’s disease (AD) is a devastating age-related neurodegenerative disorder with an alarming increasing prevalence. Except for the recently FDA-approved Aducanumab of which the therapeutic effect is not yet conclusively proven, only symptomatic medication that is effective for some AD patients is available. In order to be able to design more rational and effective treatments, our understanding of the mechanisms behind the pathogenesis and progression of AD urgently needs to be improved. Over the last years, it became increasingly clear that peripheral inflammation is one of the detrimental factors that can contribute to the disease. Here, we discuss the current understanding of how systemic and intestinal (referred to as the gut-brain axis) inflammatory processes may affect brain pathology, with a specific focus on AD. Moreover, we give a comprehensive overview of the different preclinical as well as clinical studies that link peripheral Inflammation to AD initiation and progression. Altogether, this review broadens our understanding of the mechanisms behind AD pathology and may help in the rational design of further research aiming to identify novel therapeutic targets.

scholarly journals The autophagy activator Spermidine ameliorates Alzheimer’s disease pathology and neuroinflammation in mice

2020 ◽  
Author(s):  
Kiara Freitag ◽  
Nele Sterczyk ◽  
Julia Schulz ◽  
Judith Houtman ◽  
Lara Fleck ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Inflammatory Response ◽  
Glial Cells ◽  
Oral Treatment ◽  
Small Body ◽  
Phosphorylated Tau ◽  
Inflammatory Processes ◽  
Late Stages ◽  
Inflammasome Activity

AbstractDeposition of amyloid beta (Aβ) and phosphorylated Tau along with microglia- and astrocyte-mediated neuroinflammation are prominent pathogeneic features of Alzheimer’s Disease (AD). In recent years, impairment of autophagy has also been shown to contribute to AD progression. Here, we provide evidence that oral treatment of amyloid-prone AD-like APPPS1 mice with the autophagy activator Spermidine, a small body-endogenous polyamine often used as dietary supplement, decreased neuroinflammation and reduced neurotoxic soluble Aβ at both early and late stages of AD. Mechanistically, Spermidine induced autophagy in microglia as well as in astrocytes, which subsequently impacted TLR3- and TLR4-mediated inflammatory processes by decreasing cytotoxicity, inflammasome activity and NF-κB signalling. Our data highlight that autophagy targets the inflammatory response of glial cells and emphasize the potential of orally administered autophagy-activating drugs such as Spermidine to interfere with AD progression.

Exploring the Anti-Neuroinflammatory Potential of Steroid and Terpenoid-Derived Phytochemicals to Combat Alzheimer's Disease

2021 ◽  
Vol 26 ◽  
Author(s):  
Md. Tanvir Kabir ◽  
Md. Sahab Uddin ◽  
Sonia Zaman ◽  
Md. Sohanur Rahman ◽  
Tapan Behl ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neurodegenerative Disorder ◽  
Symptomatic Treatment ◽  
Drug Candidates ◽  
Age Related ◽  
Inflammatory Processes ◽  
Pharmacologically Active ◽  
And Behavior ◽  
Therapeutic Activities

: Alzheimer's disease (AD) is an age-related progressive neurodegenerative disorder that significantly affects cognitive functions in a way that causes loss of memory, thinking, and behavior. Multiple studies revealed that neuroinflammation associated with AD is linked with the amyloid-beta deposition in the brain. Elevated levels of expression of cytokines, microglial activation, nuclear factor kappa B, and reactive oxygen species play roles in ADrelated inflammatory processes. Indeed, effective therapeutic approaches are urgently required to develop therapeutic agents to prevent and treat AD. So far, many anti-AD drug candidates have failed in the clinical stages and currently available drugs only provide symptomatic treatment. In recent times, pharmacologically active phytochemicals have been found to possess promising anti-neuroinflammatory effects; therefore these natural products can be useful in the AD treatment. In this review, we have comprehensively discussed the role of neuroinflammation and the molecular processes altered by multiple steroid and terpenoid-derived phytochemicals in various AD-related neuroinflammatory pathways. Indeed, steroid and terpenoid-derived phytochemicals show important therapeutic activities, which can be useful in ameliorating and treating AD-related neurodegeneration.

Interferon Gamma +874 T/A Gene Polymorphism is not a Risk Factor in the Pathogenesis of Alzheimer’s Disease

2009 ◽  
Vol 24 (S1) ◽  
pp. 1-1 ◽  
Author(s):  
A. Juhász ◽  
Á. Fehér ◽  
Á. Rimanóczy ◽  
J. Kálmán ◽  
Z. Janka
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Risk Factor ◽  
Gene Polymorphism ◽  
Interferon Gamma ◽  
Amyloid Beta ◽  
Simultaneous Occurrence ◽  
Healthy Controls ◽  
Inflammatory Processes

Inflammatory processes seem to play a role in neurodegenerative diseases such as Alzheimer's disease (AD). Local inflammatory mechanisms can affect to neurotoxicity, interfere with beta amyloid expression and metabolism. The increased production of amyloid precursor protein eventually leads to the deposition of amyloid beta. Interferon (INF) gamma plays a pivotal role in the inflammatory processes.The aim of this study was to evaluate the putative role of INF gamma +874 T/A polymorphism and its association with apolipoprotein E (ApoE) 4 allele in AD.One hundred and eighty nine healthy controls (HC) and 191 patients with AD were involved in this study. The probable AD patients were diagnosed by NINCDS-ADRDA criteria. The DNA was extracted from whole peripheral blood. INF gamma +874 T/A and ApoE polymorphisms were assessed by the PCR based method.ApoE 4 allele occurrence in AD was 27% compared to 9% in HC. There were no statistically significant differences in the distribution of INF gamma genotypes (AD: A/A:30.9%, T/A:46.1%, T/T:23.0%; HC: A/A:21.7%, T/A:54.5%, T/T:23.8%, p=0.110) or alleles. The INF gamma A/A genotype was more frequent in the presence of ApoE 4 allele in AD (13.6%) than in the HC (4.8%).Our results confirm the role of ApoE 4 allele in AD. However, no association was found between the INF gamma +874 T /A polymorphism and AD. The simultaneous occurrence of ApoE 4 allele and one of the INF gamma genotypes presumably can not modify the risk for AD. (ETT 198/04/2006 and OTKA K 60589/2006).

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