Synaptic mitochondrial dysfunction and septin accumulation are linked to complement-mediated synapse loss in an Alzheimer's disease animal model
BA Györffy, V Tóth, G Török, P Gulyássy… - Cellular and Molecular …, 2020 - Springer
Synaptic functional disturbances with concomitant synapse loss represent central
pathological hallmarks of Alzheimer's disease. Excessive accumulation of cytotoxic amyloid …
pathological hallmarks of Alzheimer's disease. Excessive accumulation of cytotoxic amyloid …
Complement C1q-dependent excitatory and inhibitory synapse elimination by astrocytes and microglia in Alzheimer's disease mouse models
Microglia and complement can mediate neurodegeneration in Alzheimer's disease (AD). By
integrative multi-omics analysis, here we show that astrocytic and microglial proteins are …
integrative multi-omics analysis, here we show that astrocytic and microglial proteins are …
Complement-mediated synapse loss in Alzheimer's disease: mechanisms and involvement of risk factors
L Wen, D Bi, Y Shen - Trends in Neurosciences, 2024 - cell.com
The complement system is increasingly recognized as a key player in the synapse loss and
cognitive impairments observed in Alzheimer's disease (AD). In particular, the process of …
cognitive impairments observed in Alzheimer's disease (AD). In particular, the process of …
Synaptic dysfunction and septin protein family members in neurodegenerative diseases
M Marttinen, KMA Kurkinen, H Soininen… - Molecular …, 2015 - Springer
Cognitive decline and disease progression in different neurodegenerative diseases typically
involves synaptic dysfunction preceding the neuronal loss. The synaptic dysfunction is …
involves synaptic dysfunction preceding the neuronal loss. The synaptic dysfunction is …
Terminal complement pathway activation drives synaptic loss in Alzheimer's disease models
Complement is involved in developmental synaptic pruning and pathological synapse loss
in Alzheimer's disease. It is posited that C1 binding initiates complement activation on …
in Alzheimer's disease. It is posited that C1 binding initiates complement activation on …
Proteomic and functional alterations in brain mitochondria from Tg2576 mice occur before amyloid plaque deposition
F Gillardon, W Rist, L Kussmaul, J Vogel, M Berg… - …, 2007 - Wiley Online Library
Synaptic dysfunction is an early event in Alzheimer's disease patients and has also been
detected in transgenic mouse models. In the present study, we analyzed proteomic changes …
detected in transgenic mouse models. In the present study, we analyzed proteomic changes …
[HTML][HTML] Insight into the role of phosphatidylserine in complement-mediated synapse loss in Alzheimer's disease
The innate immune system plays an integral role in the brain. Synaptic pruning, a
fundamental process in developmental circuit refinement, is partially mediated by …
fundamental process in developmental circuit refinement, is partially mediated by …
The synaptic proteome in Alzheimer's disease
RYK Chang, AS Nouwens, PR Dodd… - Alzheimer's & Dementia, 2013 - Elsevier
Background Synaptic dysfunction occurs early in Alzheimer's disease (AD) and is
recognized to be a primary pathological target for treatment. Synapse degeneration or …
recognized to be a primary pathological target for treatment. Synapse degeneration or …
Alzheimer's disease as a synaptopathy: Evidence for dysfunction of synapses during disease progression
The synapse has consistently been considered a vulnerable and critical target within
Alzheimer's disease, and synapse loss is, to date, one of the main biological correlates of …
Alzheimer's disease, and synapse loss is, to date, one of the main biological correlates of …
Synaptic pathology: a shared mechanism in neurological disease
CM Henstridge, E Pickett, TL Spires-Jones - Ageing research reviews, 2016 - Elsevier
Synaptic proteomes have evolved a rich and complex diversity to allow the exquisite control
of neuronal communication and information transfer. It is therefore not surprising that many …
of neuronal communication and information transfer. It is therefore not surprising that many …