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000163733 0247_ $$2doi$$a10.1016/S1474-4422(22)00027-8
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000163733 0247_ $$2ISSN$$a1474-4422
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000163733 037__ $$aDZNE-2022-00472
000163733 041__ $$aEnglish
000163733 082__ $$a610
000163733 1001_ $$0P:(DE-2719)2812759$$aMorenas-Rodríguez, Estrella$$b0$$eFirst author$$udzne
000163733 245__ $$aSoluble TREM2 in CSF and its association with other biomarkers and cognition in autosomal-dominant Alzheimer's disease: a longitudinal observational study.
000163733 260__ $$aLondon$$bLancet Publ. Group$$c2022
000163733 3367_ $$2DRIVER$$aarticle
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000163733 500__ $$a(CC BY-NC-ND)
000163733 520__ $$aTherapeutic modulation of TREM2-dependent microglial function might provide an additional strategy to slow the progression of Alzheimer's disease. Although studies in animal models suggest that TREM2 is protective against Alzheimer's pathology, its effect on tau pathology and its potential beneficial role in people with Alzheimer's disease is still unclear. Our aim was to study associations between the dynamics of soluble TREM2, as a biomarker of TREM2 signalling, and amyloid β (Aβ) deposition, tau-related pathology, neuroimaging markers, and cognitive decline, during the progression of autosomal dominant Alzheimer's disease.We did a longitudinal analysis of data from the Dominantly Inherited Alzheimer Network (DIAN) observational study, which includes families with a history of autosomal dominant Alzheimer's disease. Participants aged over 18 years who were enrolled in DIAN between Jan 1, 2009, and July 31, 2019, were categorised as either carriers of pathogenic variants in PSEN1, PSEN2, and APP genes (n=155) or non-carriers (n=93). We measured amounts of cleaved soluble TREM2 using a novel immunoassay in CSF samples obtained every 2 years from participants who were asymptomatic (Clinical Dementia Rating [CDR]=0) and annually for those who were symptomatic (CDR>0). CSF concentrations of Aβ40, Aβ42, total tau (t-tau), and tau phosphorylated on threonine 181 (p-tau) were measured by validated immunoassays. Predefined neuroimaging measurements were total cortical uptake of Pittsburgh compound B PET (PiB-PET), cortical thickness in the precuneus ascertained by MRI, and hippocampal volume determined by MRI. Cognition was measured using a validated cognitive composite (including DIAN word list test, logical memory delayed recall, digit symbol coding test [total score], and minimental status examination). We based our statistical analysis on univariate and bivariate linear mixed effects models.In carriers of pathogenic variants, a high amyloid burden at baseline, represented by low CSF Aβ42 (β=-4·28 × 10-2 [SE 0·013], p=0·0012), but not high cortical uptake in PiB-PET (β=-5·51 × 10-3 [0·011], p=0·63), was the only predictor of an augmented annual rate of subsequent increase in soluble TREM2. Augmented annual rates of increase in soluble TREM2 were associated with a diminished rate of decrease in amyloid deposition, as measured by Aβ42 in CSF (r=0·56 [0·22], p=0·011), in presymptomatic carriers of pathogenic variants, and with diminished annual rate of increase in PiB-PET (r=-0·67 [0·25], p=0·0060) in symptomatic carriers of pathogenic variants. Presymptomatic carriers of pathogenic variants with annual rates of increase in soluble TREM2 lower than the median showed a correlation between enhanced annual rates of increase in p-tau in CSF and augmented annual rates of increase in PiB-PET signal (r=0·45 [0·21], p=0·035), that was not observed in those with rates of increase in soluble TREM2 higher than the median. Furthermore, presymptomatic carriers of pathogenic variants with rates of increase in soluble TREM2 above or below the median had opposite associations between Aβ42 in CSF and PiB-PET uptake when assessed longitudinally. Augmented annual rates of increase in soluble TREM2 in presymptomatic carriers of pathogenic variants correlated with decreased cortical shrinkage in the precuneus (r=0·46 [0·22]), p=0·040) and diminished cognitive decline (r=0·67 [0·22], p=0·0020).Our findings in autosomal dominant Alzheimer's disease position the TREM2 response within the amyloid cascade immediately after the first pathological changes in Aβ aggregation and further support the role of TREM2 on Aβ plaque deposition and compaction. Furthermore, these findings underpin a beneficial effect of TREM2 on Aβ deposition, Aβ-dependent tau pathology, cortical shrinkage, and cognitive decline. Soluble TREM2 could, therefore, be a key marker for clinical trial design and interpretation. Efforts to develop TREM2-boosting therapies are ongoing.German Research Foundation, US National Institutes of Health.
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000163733 650_7 $$2NLM Chemicals$$aAmyloid beta-Peptides
000163733 650_7 $$2NLM Chemicals$$aBiomarkers
000163733 650_7 $$2NLM Chemicals$$aMembrane Glycoproteins
000163733 650_7 $$2NLM Chemicals$$aReceptors, Immunologic
000163733 650_7 $$2NLM Chemicals$$aTREM2 protein, human
000163733 650_2 $$2MeSH$$aAdult
000163733 650_2 $$2MeSH$$aAlzheimer Disease: diagnostic imaging
000163733 650_2 $$2MeSH$$aAlzheimer Disease: genetics
000163733 650_2 $$2MeSH$$aAmyloid beta-Peptides
000163733 650_2 $$2MeSH$$aBiomarkers
000163733 650_2 $$2MeSH$$aCognition: physiology
000163733 650_2 $$2MeSH$$aCognitive Dysfunction: diagnostic imaging
000163733 650_2 $$2MeSH$$aCognitive Dysfunction: genetics
000163733 650_2 $$2MeSH$$aHumans
000163733 650_2 $$2MeSH$$aMembrane Glycoproteins: cerebrospinal fluid
000163733 650_2 $$2MeSH$$aMembrane Glycoproteins: genetics
000163733 650_2 $$2MeSH$$aMiddle Aged
000163733 650_2 $$2MeSH$$aReceptors, Immunologic: genetics
000163733 650_2 $$2MeSH$$aUnited States
000163733 7001_ $$aLi, Yan$$b1
000163733 7001_ $$0P:(DE-2719)9000236$$aNuscher, Brigitte$$b2$$udzne
000163733 7001_ $$aFranzmeier, Nicolai$$b3
000163733 7001_ $$aXiong, Chengjie$$b4
000163733 7001_ $$0P:(DE-2719)2811727$$aSuarez-Calvet, Marc$$b5$$udzne
000163733 7001_ $$aFagan, Anne M$$b6
000163733 7001_ $$aSchultz, Stephanie$$b7
000163733 7001_ $$aGordon, Brian A$$b8
000163733 7001_ $$aBenzinger, Tammie L S$$b9
000163733 7001_ $$aHassenstab, Jason$$b10
000163733 7001_ $$aMcDade, Eric$$b11
000163733 7001_ $$0P:(DE-2719)2812867$$aFeederle, Regina$$b12$$udzne
000163733 7001_ $$aKarch, Celeste M$$b13
000163733 7001_ $$0P:(DE-2719)2812546$$aSchlepckow, Kai$$b14$$udzne
000163733 7001_ $$aMorris, John C$$b15
000163733 7001_ $$0P:(DE-2719)9000907$$aKleinberger, Gernot$$b16$$udzne
000163733 7001_ $$aNellgard, Bengt$$b17
000163733 7001_ $$0P:(DE-2719)2811820$$aVöglein, Jonathan$$b18$$udzne
000163733 7001_ $$aBlennow, Kaj$$b19
000163733 7001_ $$aZetterberg, Henrik$$b20
000163733 7001_ $$0P:(DE-2719)9000543$$aEwers, Michael$$b21$$udzne
000163733 7001_ $$0P:(DE-2719)2000010$$aJucker, Mathias$$b22$$udzne
000163733 7001_ $$0P:(DE-2719)2811659$$aLevin, Johannes$$b23$$udzne
000163733 7001_ $$aBateman, Randall J$$b24
000163733 7001_ $$0P:(DE-2719)2202037$$aHaass, Christian$$b25$$eLast author$$udzne
000163733 7001_ $$aNetwork, Dominantly Inherited Alzheimer$$b26$$eCollaboration Author
000163733 7001_ $$aAdams, Sarah$$b27
000163733 7001_ $$aAllegri, Ricardo$$b28
000163733 7001_ $$aAraki, Aki$$b29
000163733 7001_ $$aBarthelemy, Nicolas$$b30
000163733 7001_ $$aBechara, Jacob$$b31
000163733 7001_ $$aBerman, Sarah$$b32
000163733 7001_ $$aBodge, Courtney$$b33
000163733 7001_ $$aBrandon, Susan$$b34
000163733 7001_ $$aBrooks, William Bill$$b35
000163733 7001_ $$aBrosch, Jared$$b36
000163733 7001_ $$aBuck, Jill$$b37
000163733 7001_ $$aBuckles, Virginia$$b38
000163733 7001_ $$aCarter, Kathleen$$b39
000163733 7001_ $$aCash, Lisa$$b40
000163733 7001_ $$aChen, Charlie$$b41
000163733 7001_ $$aChhatwal, Jasmeer$$b42
000163733 7001_ $$aChrem, Patricio$$b43
000163733 7001_ $$aChua, Jasmin$$b44
000163733 7001_ $$aChui, Helena$$b45
000163733 7001_ $$aCruchaga, Carlos$$b46
000163733 7001_ $$aDay, Gregory S$$b47
000163733 7001_ $$aDe La Cruz, Chrismary$$b48
000163733 7001_ $$aDenner, Darcy$$b49
000163733 7001_ $$aDiffenbacher, Anna$$b50
000163733 7001_ $$aDincer, Aylin$$b51
000163733 7001_ $$aDonahue, Tamara$$b52
000163733 7001_ $$aDouglas, Jane$$b53
000163733 7001_ $$aDuong, Duc$$b54
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