C K Combs
Overview
Explore the profile of C K Combs including associated specialties, affiliations and a list of published articles.
Author names and details appear as published. Due to indexing inconsistencies, multiple individuals may share a name, and a single author may have variations. MedLuna displays this data as publicly available, without modification or verification
Snapshot
Snapshot
Articles
10
Citations
970
Followers
0
Related Specialties
Related Specialties
Top 10 Co-Authors
Top 10 Co-Authors
Published In
Affiliations
Affiliations
Soon will be listed here.
Recent Articles
1.
Floden A, Combs C
J Neurosci Methods
. 2007 Jun;
164(2):218-24.
PMID: 17553568
In vitro culture of rodent microglia is a common system used to model proinflammatory changes in the brain. However, typical postnatal brain isolation protocols are time consuming and cell numbers...
2.
Sondag C, Combs C
J Neurochem
. 2006 Mar;
97(2):449-61.
PMID: 16539666
Beta amyloid peptide-containing neuritic plaques are a defining feature of Alzheimer's disease pathology. Beta amyloid are 38-43 residue peptides derived by proteolytic cleavage of amyloid precursor protein. Although much attention...
3.
Combs C, Bates P, Karlo J, Landreth G
Neurochem Int
. 2001 Oct;
39(5-6):449-57.
PMID: 11578780
Amyloid deposition within the brains of Alzheimer's Disease patients results in the activation of microglial cells and the induction of a local inflammatory response. The interaction of microglia or monocytes...
4.
Combs C, Karlo J, Kao S, Landreth G
J Neurosci
. 2001 Feb;
21(4):1179-88.
PMID: 11160388
Reactive microglia associated with the beta-amyloid plaques in Alzheimer's disease (AD) brains initiate a sequence of inflammatory events integral to the disease process. We have observed that fibrillar beta-amyloid peptides...
5.
Combs C, Johnson D, Karlo J, Cannady S, Landreth G
J Neurosci
. 2000 Jan;
20(2):558-67.
PMID: 10632585
Alzheimer's disease (AD) is characterized by the extracellular deposition of beta-amyloid fibrils within the brain and the subsequent association and phenotypic activation of microglial cells associated with the amyloid plaque....
6.
Fitch M, Doller C, Combs C, Landreth G, Silver J
J Neurosci
. 1999 Sep;
19(19):8182-98.
PMID: 10493720
Post-traumatic cystic cavitation, in which the size and severity of a CNS injury progress from a small area of direct trauma to a greatly enlarged secondary injury surrounded by glial...
7.
Combs C, Johnson D, Cannady S, Lehman T, Landreth G
J Neurosci
. 1999 Jan;
19(3):928-39.
PMID: 9920656
Microglial interaction with amyloid fibrils in the brains of Alzheimer's and prion disease patients results in the inflammatory activation of these cells. We observed that primary microglial cultures and the...
8.
McDonald D, Bamberger M, Combs C, Landreth G
J Neurosci
. 1998 Jun;
18(12):4451-60.
PMID: 9614222
The senile plaques of Alzheimer's disease are foci of local inflammatory responses, as evidenced by the presence of acute phase proteins and oxidative damage. Fibrillar forms of beta-amyloid (Abeta), which...
9.
Combs C, Coleman P, OBanion M
Brain Res Dev Brain Res
. 1998 May;
107(1):143-58.
PMID: 9602100
Attempts to describe a mechanism of neurofibrillary tangle formation often focus on site specific phosphorylations of tau protein. These have typically been described in both Alzheimer's disease and developing brains....
10.
Song J, Combs C, Pilcher W, Song L, Utal A, Coleman P
Neurobiol Aging
. 1997 Dec;
18(5):475-81.
PMID: 9390773
A rapid reversible tau phosphorylation at Ser 396/404 was observed in adult human cortical biopsy tissue and rat primary cortical cell cultures. Tau phosphorylation increased usually during the first 20-30...