A5059594878- Alzheimer's disease research and treatments
- Amino Acid Enzymes and Metabolism
- Nicotinic Acetylcholine Receptors Study
- Supramolecular Self-Assembly in Materials
- Neurological Disease Mechanisms and Treatments
- Cholinesterase and Neurodegenerative Diseases
- Neuroinflammation and Neurodegeneration Mechanisms
VA Greater Los Angeles Healthcare System
2019-2024
Geriatric Research Education and Clinical Center
2019
Amyloid fibrils of tau are increasingly accepted as a cause neuronal death and brain atrophy in Alzheimer's disease (AD). Diminishing aggregation is promising strategy the search for efficacious AD therapeutics. Previously, our laboratory designed six-residue, nonnatural amino acid inhibitor D-TLKIVW peptide (6-DP), which can prevent vitro. However, it cannot block cell-to-cell transmission aggregation. Here, we find D-TLKIVWC (7-DP), d-cysteine extension 6-DP, not only prevents but also...
Abstract Introduction The neuronal mechanism driving Alzheimer's disease (AD) is incompletely understood. Methods Immunohistochemistry, pharmacology, biochemistry, and behavioral testing are employed in two pathological contexts—AD a transgenic mouse model—to investigate T14, 14mer peptide, as key signaling molecule the neuropathology. Results T14 increases AD brains progresses conspicuous 5XFAD mice, where its immunoreactivity corresponds to that seen AD: neurons immunoreactive for...
Alzheimer's disease (AD) and mixed dementia (MxD) comprise the majority of cases in growing global aging population. MxD describes coexistence AD pathology with vascular pathology, including cerebral small vessel (SVD). Cardiovascular increases risk for MxD, but mechanistic synergisms between coexisting pathologies affecting risk, progression ultimate clinical manifestations remain elusive. To explore additive or synergistic interactions chronic hypertension, we developed a rat model...