Featured Publications
Imaging and optogenetic modulation of vascular mural cells in the live brain
Tong L, Hill RA, Damisah EC, Murray KN, Yuan P, Bordey A, Grutzendler J. Imaging and optogenetic modulation of vascular mural cells in the live brain. Nature Protocols 2020, 16: 472-496. PMID: 33299155, DOI: 10.1038/s41596-020-00425-w.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsRegional cerebral blood flowMural cellsBlood-brain barrier maintenanceCerebral ischemia mouse modelAge-related neurodegenerative diseasesCerebral blood flowSmooth muscle cell physiologyBrain blood vesselsIschemia mouse modelVascular mural cellsBrain microvesselsHigh-resolution intravital imagingVascular disordersMouse modelBlood flowMuscle cell physiologyTransgenic miceCalcium transientsAlzheimer's diseaseCalcium imagingCell subtypesBarrier maintenanceNeurodegenerative diseasesTwo-photon optogeneticsBlood vessels
2022
Oligodendroglial macroautophagy is essential for myelin sheath turnover to prevent neurodegeneration and death
Aber ER, Griffey CJ, Davies T, Li AM, Yang YJ, Croce KR, Goldman JE, Grutzendler J, Canman JC, Yamamoto A. Oligodendroglial macroautophagy is essential for myelin sheath turnover to prevent neurodegeneration and death. Cell Reports 2022, 41: 111480. PMID: 36261002, PMCID: PMC9639605, DOI: 10.1016/j.celrep.2022.111480.Peer-Reviewed Original ResearchConceptsCell typesLive-cell imagingNeurodegenerative disease pathophysiologySuch cell typesMouse geneticsAdult-onset neurodegenerative diseaseMacroautophagyCell imagingNeurodegenerative diseasesMyelin proteinsNeurodegenerationDisease pathophysiologyTurnoverMature oligodendrocytesCentral nervous systemAmphisomesMyelin sheath structureNeural functionNervous systemMyelin turnoverGeneticsMyelin sheathProgressive motor declineProteinHomeostasis
2015
Massive accumulation of luminal protease-deficient axonal lysosomes at Alzheimer’s disease amyloid plaques
Gowrishankar S, Yuan P, Wu Y, Schrag M, Paradise S, Grutzendler J, De Camilli P, Ferguson SM. Massive accumulation of luminal protease-deficient axonal lysosomes at Alzheimer’s disease amyloid plaques. Proceedings Of The National Academy Of Sciences Of The United States Of America 2015, 112: e3699-e3708. PMID: 26124111, PMCID: PMC4507205, DOI: 10.1073/pnas.1510329112.Peer-Reviewed Original ResearchConceptsAmyloid plaquesNeuronal lysosomesAlzheimer's diseaseAlzheimer's disease brain pathologyLysosome accumulationAlzheimer's disease (AD) amyloid plaquesΒ-amyloid depositionΒ-amyloid depositsAmyloid precursor proteinLysosome-like organellesRetrograde axonal transportWild-type brainsSuch axonsSwollen axonsMassive accumulationAxonal lysosomesBrain pathologyAmyloidogenic processingMouse modelAmyloid depositsLuminal proteasesAxonal transportLocal impairmentNeuronal processesNeurodegenerative diseases
2001
Cholinesterase Inhibitors for Alzheimer’s Disease
Grutzendler J, Morris J. Cholinesterase Inhibitors for Alzheimer’s Disease. Drugs 2001, 61: 41-52. PMID: 11217870, DOI: 10.2165/00003495-200161010-00005.Peer-Reviewed Original ResearchConceptsAlzheimer's diseaseCholinesterase inhibitorsCommon age-related neurodegenerative diseaseDifferent safety profilesAvailability of acetylcholineUrgent public health problemAge-related neurodegenerative diseasesModerate Alzheimer's diseasePublic health problemPossible adverse effectsPrimary therapySymptomatic treatmentSafety profileChEIsCentral synapsesClinical experienceUS FoodDrug AdministrationHealth problemsBasic neurobiologyCognitive statusNeurodegenerative diseasesPatientsDiseaseAdverse effects