Abstract
Alzheimer’s disease (AD) is the most common form of dementia, which causes abnormalities in learning, thinking, memory, as well as behavior. Generally, symptoms of AD develop gradually and aggravate over time, and consequently severely interfere with daily activities. Furthermore, obesity is one of the common risk factors for dementia. Dysregulation of adipokine and adipocyte dysfunction are assumed to be accountable for the high risk of obesity in people that develop many related disorders such as AD. Moreover, it has been observed that the dysfunction of adipose is connected with changes in brain metabolism, brain atrophy, cognitive decline, impaired mood, neuroinflammation, impaired insulin signaling, and neuronal dysfunction in people with obesity. Conversely, the pathological mechanisms, as well as the molecular players which are involved in this association, have been unclear until now. In this article, we discuss the impact of adiponectin (AdipoQ) on obesity-related Alzheimer’s dementia.
Highlights
Alzheimer’s disease (AD) is the most frequent type of dementia among elderly individuals (Kabir et al, 2020a; Uddin et al, 2020d)
This study found that 20 years before dementia diagnosis, increased body mass index (BMI) was strongly related to a higher risk of dementia in mid-life
Modulates synaptic plasticity in the hippocampal dentate gyrus Enhances neurite outgrowth and synaptic complexity AdipoQ deficiency causes AD-like synapse loss and memory impairment Prevents Aβ42-induced apoptosis, neurotoxicity, tau phosphorylation, and neurodegeneration AdipoQ deficiency leads to memory dysfunction and AD-like pathologies Reduces neuroinflammation and depressive-like behaviors Anti-inflammatory and anti-oxidant actions on microglia
Summary
Alzheimer’s disease (AD) is the most frequent type of dementia among elderly individuals (Kabir et al, 2020a; Uddin et al, 2020d). Aged AdipoQ-deficient mice recapitulate various features of AD pathology, such as increased levels of Aβ, synapse loss, neuroinflammation, tau hyperphosphorylation, neuronal cell death, and reduced insulin signaling.
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