JNNP: Mild cognitive impairment and neurological inflammation and cerebrovascular disease in patients with Alzheimer's disease.

Small vascular disease (SVD) and neuroinvestitis are increasingly believed to be the main causes of Alzheimer's disease (AD) and other neurodegenerative diseases.
both SVD and neuro-inflammation have been shown to promote neurodegeneration and exacerbate its clinical consequences, although their pathophysiological mechanisms remain unclear.
nerve inflammation plays a central role in AD and is gradually considered an early clinical symptom in its pathogenesis.
normally, inflammation acts as a natural physiological defense against infection and injury, thus acting as a nerve protection.
usually, the immune response goes through an activation process in which small glial cells are activated to fight the infection, then the infection subsides and the small glial cells return to a "static" state.
However, this process may fail, leading to chronic inflammatory conditions characterized by the continued activeness of small glial cells and excessive, dysfunctional cytokine production, which can have harmful effects on brain tissue, endothor function and cerebrovascular networks.
the study, PK11195 electron emission fault scans (PET) were used to examine the association between SVD and neuro-inflammatory measurements of the central nervous system in the body and to analyze the overall severity and regional distribution of these biomarkers.
: 42 participants were recruited (14 healthy controls, 14 mild Alzheimer's disease, 14 amyloid-positive mild cognitive impairments, according to NIA-AA guidelines).
the neuroinstration was evaluated using the PK11195 PET imaging (a marker of small glial cell activation).
to quantify SVD, the authors evaluated white mass high strength (WMH), enlarged space around blood vessels, micro-bleeding of the brain, and cavity gaps.
the overall SVD level, the combined score of SVD subsypes of hypertension artery disease and cerebral amyloid vascular disease (CAA).
general linear model examined the association between SVD and PK11195, adjusted gender, age, education, cognition, scan interval, and corrected the error detection rate (FDR) several times.
results: PK11195 fusion results were associated with SVD markers, especially in the characteristic areas of hypertension arterial lesions: deep micro-bleeding (beta=0.63, F (1,35)=35.24,p-lt;0.001), WMH (beta=0.59,t=4.91,p.001).
analysis of the overall binding of the PK11195 and 28 of the 37 areas of interest, in particular the combination of the inner temporal lobe of the PK11195, the hypertension artery score was better than CAA (beta s 0.66-0.76, t s 3.90-5.58, F THE DR-corrected p (pFDR) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
glial cell activation is associated with SVD, especially with the subtype of hypertensive artery disease in SVD.
further research is needed to determine causation, the authors' study suggests that targeted nerve inflammation may be a new treatment strategy for SVD.
low A, Mak E, Malpetti M, et al In vivo neuroinflammation and cerebral small vessel disease in mild thumbs-up and Alzheimer's disease Journal of Neurology, Neurosurgery and Psimsy Published Online First: 11 September 2020. doi:10.1136/jnnp-2020-323894 Source: MedSci Originals !-- End of Content Presentation -- !-- To determine whether to log in.