Harris E. Blankenship

This paper shows that loss of PFKFB2 in cardiac cells leads to electrophysiological instability, including prolonged repolarization and ventricular tachyarrhythmia, linking glycolytic regulation to heart function.

This study shows that pathogenic tau in the locus coeruleus causes hyperactivity and neuropsychiatric symptoms similar to early Alzheimer's disease in mice.

The paper investigates the role of tau in VTA dopamine neuron dysfunction in Alzheimer's disease models, finding that tau induces hyperexcitability but impairs burst firing.

The paper investigates synaptic input changes in VTA dopamine neurons of 3xTg-AD mice, finding enhanced excitatory input and reduced inhibition linked to PKC activity.

The paper examines gene expression changes in dopamine and GABA neurons during aging in mice, identifying shared and distinct molecular signatures linked to neurodegenerative disease susceptibility.

This study identifies hyperexcitability in VTA dopamine neurons of 3xTg-AD mice due to CK2-dependent SK channel dysfunction, linking it to reward-based learning deficits.

The paper identifies microglia as the primary source of MHC-I in mice and humans, showing age-related and Alzheimer's-associated increases in MHC-I expression and related receptors.

This study shows that tyrosinase-induced neuromelanin accumulation in mouse locus coeruleus neurons causes hyperactivity, transcriptional changes, and degeneration, mimicking early stages of Alzheimer's and Parkinson's disease.

The paper compares microglia isolation techniques and shows that transcription/translation inhibitors reduce ex vivo activation artifacts during cell preparation.