A5055633381- Alzheimer's disease research and treatments
- Mitochondrial Function and Pathology
- Neuroscience and Neuropharmacology Research
- Tryptophan and brain disorders
- Cholinesterase and Neurodegenerative Diseases
- Trace Elements in Health
- Prion Diseases and Protein Misfolding
- Functional Brain Connectivity Studies
Massachusetts General Hospital
2020-2024
Harvard University
2020-2024
Abstract Mitochondria contribute to shape intraneuronal Ca 2+ signals. Excessive taken up by mitochondria could lead cell death. Amyloid beta (Aβ) causes cytosolic overload, but the effects of Aβ on mitochondrial levels in Alzheimer’s disease (AD) remain unclear. Using a ratiometric indicator targeted neuronal and intravital multiphoton microscopy, we find increased associated with plaque deposition death transgenic mouse model cerebral β-amyloidosis. Naturally secreted soluble applied onto...
Reactive oxidative stress is a critical player in the amyloid beta (Aβ) toxicity that contributes to neurodegeneration Alzheimer's disease (AD). Damaged mitochondria are one of main sources reactive oxygen species and accumulate Aβ plaque-associated dystrophic neurites AD brain. Although causes neuronal vitro, this has never been directly observed vivo living mouse Here, we tested for first time whether plaques soluble oligomers induce mitochondrial surrounding neurons vivo, neurotoxic...
Abstract Background Reactive oxidative stress is a critical player in the amyloid beta (Aβ) toxicity that contributes to neurodegeneration Alzheimer’s disease (AD). Mitochondrial damage, observed AD, one of main sources reactive oxygen species. Although Aβ causes neuronal mitochondria-associated vitro , this has never been directly vivo living brain. Here, we tested whether plaques and soluble oligomers induce mitochondrial surrounding neurons neurotoxic effect can be abrogated using...
Abstract Background By using in vivo multiphoton microscopy, we have previously reported that astrocytic cytosolic resting calcium (Ca 2+ ) is globally elevated a transgenic mouse model of cerebral β‐amyloidosis (APPswe/PS1dE9) (PMID:19251629). However, this phenomenon independent the proximity astrocytes to amyloid β (Aβ) plaques. In addition, soluble Aβ oligomers (Aβo) are thought mediate neuronal toxicity by increasing and causing synapse loss. For those reasons, hypothesized Aβo, rather...