All Comments by Xiongwei Zhu
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- Could Disposing of Damaged Mitochondria Treat Alzheimer’s Disease?
- Amyloid-β peptide induces mitochondrial dysfunction by inhibition of preprotein maturation.
- Tau promotes neurodegeneration via DRP1 mislocalization in vivo.
- Mitochondrial dynamics and bioenergetic dysfunction is associated with synaptic alterations in mutant SOD1 motor neurons.
- 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.
- Caspase activation precedes and leads to tangles.
- Cancer linked to Alzheimer disease but not vascular dementia.
- Expression of beta-amyloid induced age-dependent presynaptic and axonal changes in Drosophila.
- Low uric acid levels in serum of patients with ALS: further evidence for oxidative stress?
- Overexpression of SOD-2 reduces hippocampal superoxide and prevents memory deficits in a mouse model of Alzheimer's disease.
- NO Kidding? Mitochondria Fission Protein Linked to Neurodegeneration
- AD Clinical Pipeline: Immunotherapy Woes, Dimebon Boons
- Research Brief—Flurizan Fails Final Hurdle, Company Discontinues Drug
- Accelerating amyloid-beta fibrillization reduces oligomer levels and functional deficits in Alzheimer disease mouse models.
- NO synthase 2 (NOS2) deletion promotes multiple pathologies in a mouse model of Alzheimer's disease.