Karpagam Srinivasan
Overview
Explore the profile of Karpagam Srinivasan including associated specialties, affiliations and a list of published articles.
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21
Citations
2292
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Recent Articles
1.
Srinivasan K, Friedman B, Etxeberria A, Huntley M, van der Brug M, Foreman O, et al.
Cell Rep
. 2020 Jul;
31(13):107843.
PMID: 32610143
Damage-associated microglia (DAM) profiles observed in Alzheimer's disease (AD)-related mouse models reflect an activation state that could modulate AD risk or progression. To learn whether human AD microglia (HAM) display...
2.
Schwabe T, Srinivasan K, Rhinn H
Neurobiol Dis
. 2020 Jun;
143:104962.
PMID: 32535152
Recent human genetic studies have challenged long standing hypotheses about the chain of events in Alzheimer's disease (AD), as the identification of genetic risk factors in microglial genes supports a...
3.
Meilandt W, Ngu H, Gogineni A, Lalehzadeh G, Lee S, Srinivasan K, et al.
J Neurosci
. 2020 Jan;
40(9):1956-1974.
PMID: 31980586
is an Alzheimer's disease (AD) risk gene expressed in microglia. To study the role of in a mouse model of β-amyloidosis, we compared PS2APP transgenic mice versus PS2APP mice lacking...
4.
Huntley M, Srinivasan K, Friedman B, Wang T, Yee A, Wang Y, et al.
J Neurosci
. 2019 Dec;
40(5):958-973.
PMID: 31831521
Cortical circuit activity is shaped by the parvalbumin (PV) and somatostatin (SST) interneurons that inhibit principal excitatory (EXC) neurons and the vasoactive intestinal peptide (VIP) interneurons that suppress activation of...
5.
Wu T, Dejanovic B, Gandham V, Gogineni A, Edmonds R, Schauer S, et al.
Cell Rep
. 2019 Aug;
28(8):2111-2123.e6.
PMID: 31433986
Complement pathway overactivation can lead to neuronal damage in various neurological diseases. Although Alzheimer's disease (AD) is characterized by β-amyloid plaques and tau tangles, previous work examining complement has largely...
6.
Dejanovic B, Huntley M, De Maziere A, Meilandt W, Wu T, Srinivasan K, et al.
Neuron
. 2018 Nov;
100(6):1322-1336.e7.
PMID: 30392797
Synapse loss and Tau pathology are hallmarks of Alzheimer's disease (AD) and other tauopathies, but how Tau pathology causes synapse loss is unclear. We used unbiased proteomic analysis of postsynaptic...
7.
Friedman B, Srinivasan K, Ayalon G, Meilandt W, Lin H, Huntley M, et al.
Cell Rep
. 2018 Jan;
22(3):832-847.
PMID: 29346778
Microglia, the CNS-resident immune cells, play important roles in disease, but the spectrum of their possible activation states is not well understood. We derived co-regulated gene modules from transcriptional profiles...
8.
Chang M, Srinivasan K, Friedman B, Suto E, Modrusan Z, Lee W, et al.
J Exp Med
. 2017 Aug;
214(9):2611-2628.
PMID: 28778989
Loss-of-function mutations in cause frontotemporal dementia (FTD) with transactive response DNA-binding protein of 43 kD (TDP-43)-positive inclusions and neuronal ceroid lipofuscinosis (NCL). There are no disease-modifying therapies for either FTD...
9.
Haddick P, Larson J, Rathore N, Bhangale T, Phung Q, Srinivasan K, et al.
J Alzheimers Dis
. 2017 Jan;
56(3):1037-1054.
PMID: 28106546
The common p.D358A variant (rs2228145) in IL-6R is associated with risk for multiple diseases and with increased levels of soluble IL-6R in the periphery and central nervous system (CNS). Here,...
10.
Erturk A, Mentz S, Stout E, Hedehus M, Dominguez S, Neumaier L, et al.
J Neurosci
. 2016 Sep;
36(38):9962-75.
PMID: 27656033
Unlabelled: After traumatic brain injury (TBI), neurons surviving the initial insult can undergo chronic (secondary) degeneration via poorly understood mechanisms, resulting in long-term cognitive impairment. Although a neuroinflammatory response is...