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Proteomic and Functional Analyses Reveal a Mitochondrial Dysfunction in P301L Tau Transgenic Mice*
TLDR
Tau pathology involves a mitochondrial and oxidative stress disorder possibly distinct from that caused by Aβ, and P301L tau mitochondria displayed increased vulnerability toward β-amyloid (Aβ) peptide insult, suggesting a synergistic action of tau and Aβ pathology on the mitochondria. Expand
Parkinson Phenotype in Aged PINK1-Deficient Mice Is Accompanied by Progressive Mitochondrial Dysfunction in Absence of Neurodegeneration
TLDR
Older Pink1−/− mice show increasing mitochondrial dysfunction resulting in impaired neural activity similar to PD, in absence of overt neuronal death. Expand
Amyloid β-induced Changes in Nitric Oxide Production and Mitochondrial Activity Lead to Apoptosis*
TLDR
A hypothetical sequence of pathogenic steps linking mutant APP expression and amyloid production with enhanced NO production and mitochondrial dysfunction finally leading to cell death is suggested, indicating a direct involvement of Aβ in these processes. Expand
Chronic Administration of Statins Alters Multiple Gene Expression Patterns in Mouse Cerebral Cortex
TLDR
To understand the molecular targets of statins in brain, DNA microarrays were used to identify gene expression patterns in the cerebral cortex of mice chronically treated with lovASTatin, pravastatin, and simvastatin and revealed 15 genes involved in cell growth and signaling and trafficking that were similarly changed by all three statins. Expand
Mitochondrial dysfunction, apoptotic cell death, and Alzheimer's disease.
TLDR
A hypothetical sequence of the pathogenic steps linking sporadic AD, FAD, and Abeta production with mitochondrial dysfunction, caspase pathway, and neuronal loss is emphasized. Expand
Mitochondrion-derived reactive oxygen species lead to enhanced amyloid beta formation.
TLDR
It is shown for the first time that mitochondrion-derived ROS are sufficient to trigger Aβ production in vitro and in vivo and that Aβ itself leads to mitochondrial dysfunction and increased ROS levels. Expand
Mitochondrial dysfunction: An early event in Alzheimer pathology accumulates with age in AD transgenic mice
TLDR
It is concluded that Ass dependent mitochondrial dysfunction starts already at 3 months in this AD model before extracellular deposition of Ass and progression accelerates substantially with aging. Expand
Hyperforin—a key constituent of St. John's wort specifically activates TRPC6 channels
TLDR
These findings support the role of TRPC channels in neurite extension and identify hyperforin as the first selective pharmacological tool to study TRPC6 function. Expand
Impact of aging
TLDR
It is reported that lymphocytes affected by sporadic or genetic APP and PS1 AD risk factors share an increased vulnerability to cell death and exhibit a similar cell type-specific pattern, given that enhanced vulnerability was most strongly developed in the CD4+ T-cell subtype. Expand
Hyperforin represents the neurotransmitter reuptake inhibiting constituent of hypericum extract.
TLDR
The data suggest hyperforin as the active principle of hypericum extracts in biochemical models of antidepressant activity with half-maximal inhibitory concentrations for the three synaptosomal uptake systems mentioned above. Expand
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