Microglia facilitate loss of perineuronal nets in the Alzheimer's disease brain is a research paper published in EBioMedicine (2020). On theSindex it has a DataRank of 0.852. It has been cited 292 times.
Scored on demand from live citation data
Linked data & code
DataRank reads this dataset's downstream impact straight off the citation graph — no black box, no proprietary weighting. How is this computed?
FAIR checklist signals are shown for context only and do not affect DataRank scoring.
We only score data papers we can read in full — never from an abstract alone.
Base Score Contribution
0.852
From this paper's citation signal
Citation Network Contribution
0
Citation network not refreshed for this result
This paper's DataRank is currently driven only by its base citation score. Citation network data was not refreshed for this result.
Learn more about DataRank methodology →National Institute of Neurological Disorders and Stroke
Grant: R01NS083801
National Institute of Neurological Disorders and Stroke
Grant: F31NS111882
National Institute of Neurological Disorders and Stroke
Grant: F31NS108611
National Institute on Aging
Grant: U54 AG054349
National Institute on Aging
Grant: P50AG016573
National Institute on Aging
Grant: R01AG056768
National Institute on Aging
Grant: T32AG00096
National Institute on Aging
Grant: F31AG059367
National Institute on Aging
Grant: AARF-16\u2013442762
NIA NIH HHS
Grant: RF1 AG056768
NIA NIH HHS
Grant: T32 AG000096
National Institutes of Health
Alzheimer's Association
FWCI
14.82
Citation Percentile
1.0%
Citation Trend
Fields of Study
MeSH Terms
Keywords
Sustainable Development Goals
Additional file 2 of A Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques
Additional file 2 of A Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques
Additional file 3 of A Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques
Additional file 3 of A Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques
Additional file 4 of A Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques
Additional file 4 of A Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques
Additional file 5 of A Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques
Additional file 5 of A Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques
Additional file 6 of A Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques
Additional file 6 of A Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques
Additional file 7 of A Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques
Additional file 7 of A Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques
Additional file 8 of A Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques
Additional file 8 of A Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques
Additional file 9 of A Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques
Additional file 9 of A Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques
Additional file 10 of A Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques
Additional file 10 of A Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques
Additional file 11 of A Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques
Additional file 11 of A Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques