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Minocycline reduces microglial activation and improves behavioral deficits in a transgenic model of cerebral microvascular amyloid


Year of Publication:
Contact PI Name:
William E. Van Nostrand
Contact PI Affiliation:
Department of Medicine Stony Brook University New York, New York, USA
Rong Fan, Feng Xu, Mary Lou Previti, Judianne Davis, Alicia M. Grande, John K. Robinson
Primary Reference (PubMED ID):
Funding Source:
National Institute of Neurological Disorders and Stroke (NINDS)
Study Goal and Principal Findings:

This study tested anti-inflammatory drug minocycline on Aβ levels, microglia and astrocyte activation, and behavioral cognition in an AD mouse model. Past studies have shown activated microglia and astrocytes neuroinflammation are associated with Aβ deposits and cognitive decline in Alzheimer's disease. Results from this study showed after intraperitoneal injection every other day for four weeks in twelve-month old Tg-SwDI mice, minocycline treatment had no effect on cerebral Aβ accumulation, microvascular amyloid load, or soluble oligomeric Aβ levels. Although reactive astrocyte levels were unaffected, there was a significant reduction in the numbers of activated microglial cells, reduced levels of proinflammatory IL-6, and improved performance in spatial learning memory. These finding suggest that anti-inflammatory treatment targeted for cerebral microvascular amyloid-induced microglial activation can improve cognitive deficits without altering the accumulation and distribution of Aβ.

Therapeutic Agent

Therapeutic Information:
Therapy Type:
Small Molecule
Therapeutic Agent:
Therapeutic Target:
Multi Target

Animal Model

Model Information:
Model Type:
Strain/Genetic Background:
Model Type:
Strain/Genetic Background:

Experimental Design

Is the following information reported in the study?:
Power/Sample Size Calculation
Randomized into Groups
Blinded for Treatment
Blinded for Outcome Measures
Pharmacokinetic Measures
Pharmacodynamic Measures
Toxicology Measures
ADME Measures
Route of Delivery
Duration of Treatment
Frequency of Administration
Age of Animal at the Beginning of Treatment
Age of Animal at the End of Treatment
Sex as a Biological Variable
Study Balanced for Sex as a Biological Variable
Number of Premature Deaths
Number of Excluded Animals
Statistical Plan
Genetic Background
Inclusion/Exclusion Criteria Included
Conflict of Interest


Outcome Measured
Outcome Parameters
Barnes Maze
Activated Microglia
Activated Astrocytes
beta Amyloid Deposits
beta Amyloid Load
Brain-beta Amyloid Oligomers
Brain-beta Amyloid Peptide-Total
Brain-Buffer Insoluble beta Amyloid Peptide 40
Brain-Buffer Insoluble beta Amyloid Peptide 42
Brain-Buffer Soluble beta Amyloid Peptide 40
Brain-Buffer Soluble beta Amyloid Peptide 42
Glial Fibrillary Acidic Protein (GFAP)
Interleukin 6 (IL-6)
Body Weight