All Comments by M. Flint Beal
- Could Disposing of Damaged Mitochondria Treat Alzheimer’s Disease?
- It’s MAGIC: Yeast Mitochondria Make Cytosolic Protein Aggregates Disappear
- Preventive methylene blue treatment preserves cognition in mice expressing full-length pro-aggregant human Tau.
- Amyloid-β peptide induces mitochondrial dysfunction by inhibition of preprotein maturation.
- Protein Destroying Muscle, Bone, Nerves Parks on Mitochondria
- Kynurenine 3-monooxygenase inhibition in blood ameliorates neurodegeneration.
- Impaired mitochondrial dynamics and abnormal interaction of amyloid beta with mitochondrial protein Drp1 in neurons from patients with Alzheimer's disease: implications for neuronal damage.
- Hearing Loss Linked to Incident Dementia
- Inhibition of amyloid-beta (Abeta) peptide-binding alcohol dehydrogenase-Abeta interaction reduces Abeta accumulation and improves mitochondrial function in a mouse model of Alzheimer's disease.
- Mitochondrial bioenergetic deficit precedes Alzheimer's pathology in female mouse model of Alzheimer's disease.
- Mitochondrial Gridlock—Syntaphilin Puts Brakes on Axonal Transport
- Progressive parkinsonism in mice with respiratory-chain-deficient dopamine neurons.
- DNA Deletions Sap Mitochondria in Parkinson Neurons
- A cluster of metabolic defects caused by mutation in a mitochondrial tRNA.
- Bile Acid Proves Neuroprotective in Huntington's Model