Abstract
Alzheimer’s disease is the most common neurodegenerative brain disease causing dementia. It is characterized by slow onset and gradual worsening of memory and other cognitive functions. Recently, parabiosis and infusion of plasma from young mice have been proposed to have positive effects in aging and Alzheimer’s disease. Therefore, this study examined whether infusion of plasma from exercised mice improved cognitive functions related to the hippocampus in a 3xTg-Alzheimer’s disease (AD) model. We collected plasma from young mice that had exercised for 3 months and injected 100 µL of plasma into the tail vein of 12-month-old 3xTg-AD mice 10 times at 3-day intervals. We then analyzed spatial learning and memory, long-term memory, hippocampal GSK3β/tau proteins, synaptic proteins, mitochondrial function, apoptosis, and neurogenesis. In the hippocampus of 3xTg-AD mice, infusion of plasma from exercised mice improved neuroplasticity and mitochondrial function and suppressed apoptosis, ultimately improving cognitive function. However, there was no improvement in tau hyperphosphorylation. This study showed that plasma from exercised mice could have a protective effect on cognitive dysfunction and neural circuits associated with AD via a tau-independent mechanism involving elevated brain-derived neurotrophic factor due to exercise.
Highlights
Alzheimer’s disease (AD) is the most common cause of dementia, characterized by slow onset and progressive decline of memory and cognitive functions
Cognitive dysfunction, including that involving memory and learning, is associated with decreased neurogenesis in the hippocampus, which could result from decreased expression of immature neuron factors, such as DCX, that signal the birth of new neurons [6]
In this study, we aimed to examine whether transfusion of plasma from exercised mice could have similar effects to exercise on cognitive function, hippocampal neuroplasticity, and mitochondrial function in AD
Summary
Alzheimer’s disease (AD) is the most common cause of dementia, characterized by slow onset and progressive decline of memory and cognitive functions. AD is associated with various cellular changes in the brain, including synaptic injury, alterations in mitochondrial structure and function, abnormal inflammatory response, extracellular accumulation of amyloid beta (Aβ), and intracellular neurofibrillary tangles [1,2,3]. AD is caused by atrophy, senile plaques, and hyperphosphorylated tau protein aggregates in the hippocampus, one of the neuroanatomical areas responsible for memory and learning [4,5]. Cognitive dysfunction, including that involving memory and learning, is associated with decreased neurogenesis in the hippocampus, which could result from decreased expression of immature neuron factors, such as DCX (doublecortin), that signal the birth of new neurons [6]. It has been suggested that mitochondrial dysfunction could develop when the course of AD worsens or in all stages of the disease, and that this process may occur in the brain, but systemically [13]
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