Effects of Aerobic Exercise and Resistance Training on Cognitive Function: Comparative Study Based on FNDC5/Irisin/BDNF Pathway.

Introduction: Exercise has been recommended to suppress or prevent cognitive decline. Aerobic exercise (AE) may suppress cognitive decline via the fibronectin type III domain-containing protein 5 (FNDC5)/irisin/brain-derived neurotrophic factor (BDNF) pathway, and resistance training (RT) has a preventive effect on cognitive decline. However, the underlying mechanism remains unclear.

FNDC5/irisin mediates the protective effects of Innovative theta-shaking exercise on mouse memory.

As a passive motion and non-invasive treatment, theta-shaking exercise is considered an alternative to traditional active exercise for slowing down brain ageing. Here, we studied the influence of theta-shaking exercise on fibronectin type III domain containing 5/irisin (FNDC5/irisin) in the anterior nucleus of the thalamus, hippocampus, and medial prefrontal cortex (ATN-HPC-MPFC). Further, we assessed memory in senescence-accelerated prone mice (SAMP-10 mice) using a behavioural test to confirm the protective effect of theta-shaking exercise against age-related memory decline.

Exercise through Shaking Stimuli Suppresses Cancer Growth via the Wnt pathway in ApcMin/+ Mice.

Objective: Exercise has been reported to suppress colorectal cancer; however, the mechanism of suppression by exercise and its effect on the Wnt pathway, which is particularly involved in the early stage of carcinogenesis, remain unclear. In this study, we subjected ApcMin/+ mice to exercise by shaking stimuli to investigate the mechanisms of suppressing colorectal cancer, and focused on the Ca2+ pathway, which is one of the β-catenin-independent Wnt signaling pathways that suppress the accumulation of β-catenin.

Methods: Mice in the exercise group were subjected to exercise by shaking stimuli for 30 min/session, 6 sessions/ week, for a total of 11 weeks.

Exercise by Shaking Alleviates the Decline in Memory due to Aging: A Study in Mice.

Introduction: Although exercise can prevent cognitive decline due to aging, few elderly individuals are able to exercise for long. Therefore, an exercise method for older adults that is feasible for a long duration without overexertion is necessary. In this study, we focused on exercise by shaking.

Novel shaking exercises for hippocampal and medial prefrontal cortex functioning maintain spatial working memory.

Introduction: The decline in spatial working memory is one of the earliest signs of normal brain aging.

Objective: We developed a novel physical exercise method, termed the "shaking exercise," to slow down this process.

Methods: The experimental protocol included administering the shaking exercise for 8-32 weeks in male senescence-accelerated mouse prone 10 (SAMP-10).

After haemin treatment intracellular non-haem iron increases prior to haem oxygenase-1 induction: A study in human monocytic cell line THP-1.

Background: Iron overload is a major health concern for transfusion-dependent patients. Repeated transfusions result in the loading of large amounts of haem-derived iron on macrophages, in turn, inducing cell death. We previously demonstrated that haemin-induced cell death in human monocytic THP-1 cells is consistent with ferroptosis, an iron-dependent cell death regulation mechanism.

Haemin-induced cell death in human monocytic cells is consistent with ferroptosis.

Background: Iron overload is a major issue for transfusion-dependent patients. Repeated transfusions result in the loading of large amounts of haem-derived iron on macrophages, and the haemin in turn induces cell death and the generation of reactive oxygen species (ROS) in both murine macrophages and human monocytic THP-1 cells. This haemin-induced cell death process has been shown to be iron-dependent.

Mutant huntingtin impairs Ku70-mediated DNA repair.

DNA repair defends against naturally occurring or disease-associated DNA damage during the long lifespan of neurons and is implicated in polyglutamine disease pathology. In this study, we report that mutant huntingtin (Htt) expression in neurons causes double-strand breaks (DSBs) of genomic DNA, and Htt further promotes DSBs by impairing DNA repair. We identify Ku70, a component of the DNA damage repair complex, as a mediator of the DNA repair dysfunction in mutant Htt-expressing neurons.

Neuroprotective and neurotoxic phenotypes of activated microglia in neonatal mice with respective MPTP- and ethanol-induced brain injury.

Activated microglia play important roles in the inflammatory process and progression in Parkinson's disease. These cells produce various cytokines, nitric oxide, and neurotrophins, which are pleiotropic in their action, i.e.

Water-dispersed single-wall carbon nanohorns as drug carriers for local cancer chemotherapy.

Aim: Functional analyses of water-dispersed carbon nanohorns with antitumor activity were performed to explore their potential as a drug carrier for local cancer chemotherapy.

Materials & Methods: Water-dispersed carbon nanohorns were prepared through adsorption of polyethylene glycol-doxorubicin conjugate (PEG-DXR) onto oxidized single-wall carbon nanohorns (oxSWNHs). PEG-DXR-bound oxSWNHs were administered intratumorally to human nonsmall cell lung cancer-cell NCI-H460-bearing mice.

Effects of aging on neuroprotective and neurotoxic properties of microglia in neurodegenerative diseases.

The inflammatory process in the brain, which is accompanied by changes in the levels of proinflammatory cytokines and neurotrophins, along with the presence of activated microglia, has recently gained much attention in neurodegenerative diseases. Activated microglia produce either neuroprotective or neurotoxic factors. Many reports indicate that activated microglia promote degeneration of dopamine (DA) neurons in Parkinson's disease (PD).

Activated microglia affect the nigro-striatal dopamine neurons differently in neonatal and aged mice treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine.

Microglia play an important role in the inflammatory process that occurs in Parkinson's disease (PD). Activated microglia produce cytokines and neurotrophins and may have neurotoxic or neurotrophic effects. Because microglia are most proliferative and easily activated during the neonatal period, we examined the effects of neonatal microglia activated with lipopolysaccharide (LPS) on the nigro-striatal dopamine neurons in mice treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), in comparison with activated microglia from the aged mice.

Characterization of neuron-specific huntingtin aggregates in human huntingtin knock-in mice.

Huntington's disease (HD) is caused by a mutation causing expanded polyglutamine tracts in the N-terminal fragment of huntingtin. A pathological hallmark of HD is the formation of aggregates in the striatal neurons. Here we report that ageing human huntingtin knock-in mice expressing mutant human huntingtin contained neuronal huntingtin aggregates, as revealed by immunohistochemical analysis.

Expression of erbB receptors mRNA in thyroid tissues.

ErbB family members, such as epidermal growth factor receptor 1 (erbB1), erbB2, erbB3 and erbB4, are widely distributed in organ tissues, and these receptors are suspected tumorigenesis factors. We measured erbB mRNA in thyroid tissues of benign and malignant thyroid tumors or Graves' disease using Genescan. ErbB2 is associated with aggressive cancers and is used as a biological marker for the disease; Northern blot and reverse transcription-polymerase chain reaction (RT-PCR) analyses have shown it to be increased in Graves' disease.

Identification and characterization of novel mouse and human ADAM33s with potential metalloprotease activity.

The ADAM family of membrane-anchored proteins has a unique domain structure, with each containing a disintegrin and metalloprotease (ADAM) domain. We have isolated mouse and human cDNAs encoding a novel member of the ADAM family. The mouse and human predicted proteins consisted of 797 and 813 amino acids, respectively, and they shared 70% homology of the entire amino acid sequence.