Abstract
Alzheimer’s disease (AD) is accompanied by β-amyloid (Aβ), neurofibrillary tangles, and neuron cell death, and is one of the most commonly occurring diseases among the elderly. The pathology of AD is complex, involving Aβ overproduction and accumulation, tau hyperphosphorylation, and neuronal loss. In addition, chronic cerebral hypoperfusion (CCH) is ubiquitous in the AD patients and plans a pivotal role in triggering and exacerbating the pathophysiological progress of AD. The goal of this study was to investigate the neuroprotective properties of berberine (BBR) and the underlying mechanism. During the study, BBR was administrated to treat the triple-transgenic mouse model of Alzheimer’s disease (3×Tg AD). To thoroughly evaluate the effects of the BBR administration, multiple manners were utilized, for instance, 3D arterial spin labeling technique, Morris water maze assay, immunofluorescence staining, TUNEL assay, laser speckle contrast imaging, western blotting, etc. The results showed that BBR ameliorated cognitive deficits in 3×Tg AD mice, reduced the Aβ accumulation, inhibited the apoptosis of neurons, promoted the formation of microvessels in the mouse brain by enhancing brain CD31, VEGF, N-cadherin, Ang-1. The new vessels promoted by BBR were observed to have a complete structure and perfect function, which in turn promoted the recovery of cerebral blood flow (CBF). In general, berberine is effective to 3×Tg AD mice, has a neuroprotective effect, and is a candidate drug for the multi-target prevention and treatment of AD.
Highlights
Alzheimer’s disease (AD) becomes the leading cause of dementia in the elderly
The 3D arterial spin labeling (ASL) technique was applied to detected cerebral blood flow (CBF) in every mouse across the three groups
It supports the hypothesis that BBR could accelerate the recovery of CBF in a 3×Tg AD mouse model
Summary
Alzheimer’s disease (AD) becomes the leading cause of dementia in the elderly. Characterized by chronic progressive neurodegeneration, AD results in progressive cognitive impairment and, death. The AD pathology relates to a variety of factors. The most frequent histopathological changes include the formation of neurofibrillary tangles (NFTs) and senile plaque in the brain, accompanied by neurodegeneration [1,2]. Previous research on AD did not deeply explore vascular factors. AD and vascular dementia (VD) were treated as two completely distinct diseases, degenerative diseases and vascular diseases [3,4]. Emerging evidence implies the contribution of chronic cerebral hypoperfusion (CCH) towards the pathogenesis of AD. Researchers observe the reduction of CBF in temporal, parietal and frontal cortices among
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