Serum MCP-1 levels are increased in mild cognitive impairment and mild Alzheimer's disease

Increased production of inflammatory cytokines in mild cognitive impairment

“…Paganelli et al (2002) have found that the level of serum TNF-α is significantly lower in mild-moderate AD compared to severe AD and vascular dementia suggesting a difference in the cytokine profile at different stages of AD as well as between other types of dementia. Our data support the hypothesis that inflammation is an early event rather than a late consequence of the disease (Galimberti et al, 2005;Tarkowski et al, 2003).…”

“…Increasing evidence suggests that peripheral modification of inflammatory factors may occur early during the development of AD (Galimberti et al, 2005;Huberman et al, 1994;Tarkowski et al, 2003). This may explain the results of several epidemiological studies that suggest that non-steroidal anti-inflammatory drugs (NSAIDs) protect against AD but do not have therapeutic effects (in t' Veld et al, 2001;McGeer et al, 1996;Pasinetti and Pompl, 2002).…”

“…An altered immune profile has also been found in MCI patients. Serum monocyte chemotactic protein-1 (MCP-1), a beta chemokine, was shown to be upregulated in MCI and mild AD but not in severe AD patients as compared with controls (Galimberti et al, 2005). Furthermore, both MCI and AD patients who had progressed from MCI had higher TNF-α (proinflammatory cytokine) to TGF-β (anti-inflammatory cytokine) ratios in CSF when compared to healthy controls, indicating a higher proinflammatory state in patients at risk for AD (Tarkowski et al, 2003).…”

Pyroglutamate Amyloid β (Aβ) Aggravates Behavioral Deficits in Transgenic Amyloid Mouse Model for Alzheimer Disease

“…For example, the N terminus of monocyte chemoattractant protein 1 (CCL2/MCP-1) is modified to a pyroglutamate residue, thereby protecting it against degradation (32). MCP-1 plays a pivotal role in different inflammatory conditions (33). As microglial activity could contribute to neuron dysfunction (33), a potential effect of QC overexpression on microglia-mediated inflammation in transgenic 5XFAD/hQC mice cannot be ruled out.…”

Prep1/Pbx2 complexes regulate CCL2 expression through the −2578 guanine polymorphism

“…1 Owing to its importance in inflammatory responses, increased levels of CCL2 have been implicated in a variety of disease pathologies including arthersosclerosis, cancer metastisis, multiple sclerosis, Alzheimer's disease and human immunodeficiency virus-associateddementia (HIV-D). [2][3][4][5][6][7] In other settings, CCL2 appears to be beneficial as it protects against initial HIV infection, is neuroprotective against HIV Tat and N-methyl-D-aspartate-induced apoptosis during early HIV infection, and promotes healing following myocardial infarct. [8][9][10] Genetic analysis of the distal CCL2 promoter revealed a polymorphism at À2578 (alternatively designated À2518 11 ) with functional consequences in the context of a luciferase reporter assay.…”