Michael J. Beckstead

The paper shows that cell identity and regulatory logic are preserved during brain aging, but cell-type-specific changes occur in DNA modifications and gene expression.

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.

This study finds that aged mice acquire intravenous opioid self-administration faster than young mice, with variable effects on intake and cue-responding for remifentanil but not fentanyl.

The paper compares tamoxifen-mediated cre induction efficiency and specificity in young and old mice, finding no significant difference in microglial labeling or translatomic changes.

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.

This study examines how long-term methamphetamine self-administration affects glutathione levels, mitochondrial respiration, and dopamine neuron activity in mice.

This study investigates age and sex effects on D2 autoreceptor inhibition in SNc dopamine neurons, finding reduced D2-IPSCs in aged males with preserved plasticity mechanisms.

The paper introduces a NuTRAP method to isolate RNA and DNA from specific CNS cell types, revealing cell type-specific epigenetic and transcriptomic differences in microglia and astrocytes.

This study finds that male mice show age-related decline in substantia nigra dopamine neuron firing, while females remain resilient, with increased expression of Parkinson's-related genes in males.

This study shows that deleting the neurotensin receptor 1 in mice reduces methamphetamine self-administration and prevents the decrease in dopamine neuron firing frequency associated with prolonged use.

The paper shows that neurotensin release from dopamine neurons drives long-term depression of D2R synaptic currents, which is enhanced by methamphetamine self-administration.

This study shows that VTA astrocytes regulate avoidance behavior by modulating local GABA neuron activity, which inhibits dopamine neurons and blocks reward preference.

This study shows that repeated cocaine or methamphetamine treatment reduces astrocytic markers and increases CRF2 immunoreactivity in the VTA and SN.