A5019182420- Neuroinflammation and Neurodegeneration Mechanisms
- Alzheimer's disease research and treatments
- Neurogenesis and neuroplasticity mechanisms
- Neuroscience and Neuropharmacology Research
- Immune cells in cancer
- Healthcare Policy and Management
- Tryptophan and brain disorders
- Nerve injury and regeneration
- Complement system in diseases
- Barrier Structure and Function Studies
- Primary Care and Health Outcomes
- Single-cell and spatial transcriptomics
- Nuclear Receptors and Signaling
- Genetic Neurodegenerative Diseases
- Neurological Disease Mechanisms and Treatments
- Adenosine and Purinergic Signaling
- Neural dynamics and brain function
- Retinal Development and Disorders
- Axon Guidance and Neuronal Signaling
- Immune Response and Inflammation
- Functional Brain Connectivity Studies
- Neuroscience and Neural Engineering
- Retinal Diseases and Treatments
- Neuropeptides and Animal Physiology
- Interpreting and Communication in Healthcare
Boston Children's Hospital
2016-2025
Harvard University
2016-2025
Broad Institute
2016-2025
Howard Hughes Medical Institute
2018-2025
Boston Children's Museum
2013-2025
New York Academy of Sciences
2023
John Wiley & Sons (Germany)
2023
Moss Landing Marine Laboratories
2023
Hudson Institute
2017-2023
MRC Cognition and Brain Sciences Unit
2014-2023
Too much cleaning up The complement system and microglia seek out destroy unwanted cellular debris for the peripheral immune as well excess synapses in developing brain. Hong et al. now show how may go haywire adults early progression toward Alzheimer's disease (AD). Aberrant synapse loss is an feature of correlates with cognitive decline. In mice susceptible to AD, was associated synapses, microglial function required loss. authors speculate that aberrant activation this “trash disposal”...
C3 deficiency protects against hippocampal neurodegeneration and cognitive decline in aged APP/PS1 mice despite abundant Aβ plaques.
Glaucoma is one of the most common neurodegenerative diseases. Despite this, earliest stages this complex disease are still unclear. This study was specifically designed to identify early glaucoma in DBA/2J mice. To do we used genome-wide expression profiling optic nerve head and retina a series computational methods. Eyes with no detectable by conventional assays were grouped into molecularly defined using unbiased hierarchical clustering. These represent temporally ordered sequence states....
Excessive CNS synapses are eliminated during development to establish mature patterns of neuronal connectivity. A complement cascade protein, C1q, is involved in this process. Mice deficient C1q fail refine retinogeniculate connections resulting excessive retinal innervation lateral geniculate neurons. We hypothesized that knockout (KO) mice would exhibit defects neocortical synapse elimination enhanced excitatory synaptic connectivity and epileptiform activity. recorded spontaneous evoked...
The complement system is part of the innate immune response responsible for removing pathogens and cellular debris, in addition to helping refine CNS neuronal connections via microglia-mediated pruning inappropriate synapses during brain development. However, less known about role normal aging. Here, we studied central component, C3, synaptic health We examined behavior as well electrophysiological, synaptic, changes brains C3 -deficient male mice ( KO) compared with age-, strain-,...