FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W4313702073> ?p ?o ?g. }

• W4313702073 abstract "Synaptic dysfunction is an early event in Alzheimer's disease. Post-mortem studies suggest that alterations in synaptic proteins are associated with cognitive decline in Alzheimer's disease. We measured the concentration of three synaptic proteins, zinc transporter protein 3, dynamin1 and AMPA glutamate receptor 3 in cerebrospinal fluid of subjects with mild cognitive impairment (n = 18) and Alzheimer's disease (n = 18) and compared the levels to cognitively and neurologically healthy controls (n = 18) by using ELISA assay. In addition, we aimed to assess the translational potential of these synaptic proteins in two established amyloid precursor protein knock-in Alzheimer's disease mouse models by assessing the cerebrospinal fluid, hippocampal and cortical synaptic protein concentrations. Using ELISA, we measured in parallel these three proteins in cerebrospinal fluid and/or brain of 12- and 24-month-old AppNL-F and AppNL-G-F knock-in mice and AppWt control mice. The regional distribution and expression of these proteins were explored upon aging of the App knock-in models by quantitative immunofluorescence microscopy. Notably, we found a significant increase in concentrations of zinc transporter protein 3 and AMPA glutamate receptor 3 in cerebrospinal fluid of both patient groups compared with cognitively healthy controls. Dynamin1 concentration was significantly higher in Alzheimer's disease patients. Remarkably, patients with mild cognitive impairment who converted to Alzheimer's disease (n = 7) within 2 years exhibited elevated baseline cerebrospinal fluid zinc transporter protein 3 concentrations compared with mild cognitive impairment patients who did not convert (n = 11). Interestingly, similar to the alterations in Alzheimer's disease subjects, cerebrospinal fluid AMPA glutamate receptor 3 concentration was significantly higher in AppNL-G-F knock-in mice when compared with wild-type controls. Furthermore, we have detected age and brain regional specific changes of the three synaptic proteins in the hippocampus and prefrontal cortex of both AppNL-F and AppNL-G-F knock-in mice. Notably, all the three cerebrospinal fluid synaptic protein concentrations correlated negatively with concentrations in hippocampal lysates. The elevated zinc transporter protein 3 concentrations in the cerebrospinal fluid of converter versus non-converter mild cognitive impairment patients suggests a prospective role of zinc transporter 3 in differentiating dementia patients of the biological continuum of Alzheimer's disease. The increased cerebrospinal fluid concentrations of synaptic proteins in both patient groups, potentially reflecting synaptic alterations in the brain, were similarly observed in the amyloid precursor protein knock-in mouse models highlighting the translational potential of these proteins as markers for synaptic alterations. These synaptic markers could potentially help reduce the current disparities between human and animal model-based studies aiding the translation of preclinical discoveries of pathophysiological changes into clinical research." @default.
• W4313702073 created "2023-01-08" @default.
• W4313702073 creator A5014291973 @default.
• W4313702073 creator A5016371647 @default.
• W4313702073 creator A5018503713 @default.
• W4313702073 creator A5023726732 @default.
• W4313702073 creator A5025965154 @default.
• W4313702073 creator A5045129933 @default.
• W4313702073 creator A5052814699 @default.
• W4313702073 creator A5071247507 @default.
• W4313702073 creator A5078169388 @default.
• W4313702073 date "2022-12-29" @default.
• W4313702073 modified "2023-10-17" @default.
• W4313702073 title "Translational potential of synaptic alterations in Alzheimer’s disease patients and amyloid precursor protein knock-in mice" @default.
• W4313702073 cites W1970130998 @default.
• W4313702073 cites W1978420618 @default.
• W4313702073 cites W1990300073 @default.
• W4313702073 cites W1998674695 @default.
• W4313702073 cites W2007936548 @default.
• W4313702073 cites W2013399092 @default.
• W4313702073 cites W2016087140 @default.
• W4313702073 cites W2029695041 @default.
• W4313702073 cites W2030641075 @default.
• W4313702073 cites W2031727962 @default.
• W4313702073 cites W2033629223 @default.
• W4313702073 cites W2035089473 @default.
• W4313702073 cites W2037387044 @default.
• W4313702073 cites W2049069390 @default.
• W4313702073 cites W2052226124 @default.
• W4313702073 cites W2055649795 @default.
• W4313702073 cites W2072439402 @default.
• W4313702073 cites W2073039026 @default.
• W4313702073 cites W2077122729 @default.
• W4313702073 cites W2080034260 @default.
• W4313702073 cites W2080455250 @default.
• W4313702073 cites W2088315426 @default.
• W4313702073 cites W2090620788 @default.
• W4313702073 cites W2099540110 @default.
• W4313702073 cites W2103670708 @default.
• W4313702073 cites W2115017507 @default.
• W4313702073 cites W2135957529 @default.
• W4313702073 cites W2143333161 @default.
• W4313702073 cites W2147755473 @default.
• W4313702073 cites W2151123745 @default.
• W4313702073 cites W2169135478 @default.
• W4313702073 cites W2275737843 @default.
• W4313702073 cites W2289040490 @default.
• W4313702073 cites W2508942609 @default.
• W4313702073 cites W2529533701 @default.
• W4313702073 cites W2582524520 @default.
• W4313702073 cites W2582951843 @default.
• W4313702073 cites W2733572936 @default.
• W4313702073 cites W2740213823 @default.
• W4313702073 cites W2782564735 @default.
• W4313702073 cites W2798054687 @default.
• W4313702073 cites W2899826954 @default.
• W4313702073 cites W2909351650 @default.
• W4313702073 cites W2950228559 @default.
• W4313702073 cites W3005694430 @default.
• W4313702073 cites W3025834426 @default.
• W4313702073 cites W3033804370 @default.
• W4313702073 cites W3044030235 @default.
• W4313702073 cites W3081139002 @default.
• W4313702073 cites W3084323449 @default.
• W4313702073 cites W3093654837 @default.
• W4313702073 cites W3111250940 @default.
• W4313702073 cites W3119031139 @default.
• W4313702073 cites W3159530258 @default.
• W4313702073 cites W4206774749 @default.
• W4313702073 cites W4235875658 @default.
• W4313702073 cites W4296816736 @default.
• W4313702073 doi "https://doi.org/10.1093/braincomms/fcad001" @default.
• W4313702073 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/36687391" @default.
• W4313702073 hasPublicationYear "2022" @default.
• W4313702073 type Work @default.
• W4313702073 citedByCount "0" @default.
• W4313702073 crossrefType "journal-article" @default.
• W4313702073 hasAuthorship W4313702073A5014291973 @default.
• W4313702073 hasAuthorship W4313702073A5016371647 @default.
• W4313702073 hasAuthorship W4313702073A5018503713 @default.
• W4313702073 hasAuthorship W4313702073A5023726732 @default.
• W4313702073 hasAuthorship W4313702073A5025965154 @default.
• W4313702073 hasAuthorship W4313702073A5045129933 @default.
• W4313702073 hasAuthorship W4313702073A5052814699 @default.
• W4313702073 hasAuthorship W4313702073A5071247507 @default.
• W4313702073 hasAuthorship W4313702073A5078169388 @default.
• W4313702073 hasBestOaLocation W43137020731 @default.
• W4313702073 hasConcept C104317684 @default.
• W4313702073 hasConcept C126322002 @default.
• W4313702073 hasConcept C134018914 @default.
• W4313702073 hasConcept C148762608 @default.
• W4313702073 hasConcept C149011108 @default.
• W4313702073 hasConcept C160268369 @default.
• W4313702073 hasConcept C169760540 @default.
• W4313702073 hasConcept C170493617 @default.
• W4313702073 hasConcept C185592680 @default.
• W4313702073 hasConcept C2779134260 @default.
• W4313702073 hasConcept C2779483572 @default.
• W4313702073 hasConcept C2779651940 @default.
• W4313702073 hasConcept C2781161787 @default.

• next