Journal
SEMINARS IN IMMUNOPATHOLOGY
Volume 40, Issue 1, Pages 113-124Publisher
SPRINGER HEIDELBERG
DOI: 10.1007/s00281-017-0662-9
Keywords
Complement; Neurodegeneration; Alzheimer's disease
Categories
Funding
- Wellcome Trust NIMA Consortium
- MRC
- Alzheimers Research UK [ARUK-PPG2015A-11] Funding Source: researchfish
- Alzheimer's Society [104] Funding Source: researchfish
- Medical Research Council [UKDRI-3002] Funding Source: researchfish
- MRC [UKDRI-3002] Funding Source: UKRI
Ask authors/readers for more resources
The emergence of complement as an important player in normal brain development and pathological remodelling has come as a major surprise to most scientists working in neuroscience and almost all those working in complement. That a system, evolved to protect the host against infection, should have these unanticipated roles has forced a rethink about what complement might be doing in the brain in health and disease, where it is coming from, and whether we can, or indeed should, manipulate complement in the brain to improve function or restore homeostasis. Complement has been implicated in diverse neurological and neuropsychiatric diseases well reviewed elsewhere, from depression through epilepsy to demyelination and dementia, in most complement drives inflammation to exacerbate the disease. Here, I will focus on just one disease, the most common cause of dementia, Alzheimer's disease. I will briefly review the current understanding of what complement does in the normal brain, noting, in particular, the many gaps in understanding, then describe how complement may influence the genesis and progression of pathology in Alzheimer's disease. Finally, I will discuss the problems and pitfalls of therapeutic inhibition of complement in the Alzheimer brain.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available