The understanding of the key mechanisms behind human brain deterioration in Alzheimer' disease (AD) is a highly active field of research. The most widespread hypothesis considers a cascade of events initiated by amyloid-β peptide fibrils that ultimately lead to the formation of the lethal amyloid plaques. Recent studies have shown that other agents, in particular magnetite, can also play a pivo...

SEE HANSSON AND GOURAS DOI101093/AWW146 FOR A SCIENTIFIC COMMENTARY ON THIS ARTICLE: Although some brain regions such as precuneus and lateral temporo-parietal cortex have been shown to be more vulnerable to Alzheimer's disease than other areas, a mechanism underlying the differential regional vulnerability to Alzheimer's disease remains to be elucidated. Using fluorodeoxyglucose and Pittsburgh...

β-amyloid hypothesis is the predominant hypothesis in the study of pathogenesis of Alzheimer's disease. This hypothesis claims that aggregation and neurotoxic effects of amyloid β (Aβ) is the common pathway in a variety of etiological factors for Alzheimer's disease. Aβ peptide derives from amyloid precursor protein (APP). β-sheet breaker peptides can directly prevent and reverse protein misfol...

Inactivity, obesity, and insulin resistance are significant risk factors for the development of Alzheimer's disease (AD). Several studies have demonstrated that diet-induced obesity, inactivity, and insulin resistance exacerbate the neuropathological hallmarks of AD. The aggregation of β-amyloid peptides is one of these hallmarks. β-Site amyloid precursor protein-cleaving enzyme 1 (BACE1) is th...

Previously, we demonstrated that mitochondrial bioenergetic deficits preceded Alzheimer's disease (AD) pathology in the female triple-transgenic AD (3xTgAD) mouse model. In parallel, 3xTgAD mice exhibited elevated expression of ketogenic markers, indicating a compensatory mechanism for energy production in brain. This compensatory response to generate an alternative fuel source was temporary an...

BACKGROUND Dementia induced by β-amyloid accumulation impairs peripheral glucose homeostasis, but red pepper extract improves glucose homeostasis. We therefore evaluated whether long-term oral consumption of different red pepper extracts improves cognitive dysfunction and glucose homeostasis in type 2 diabetic rats with β-amyloid-induced dementia. METHODS Male diabetic rats received hippocamp...

Aside from apolipoprotein E (APOE), genetic risk factors for β amyloid deposition in cognitively intact individuals remain to be identified. Brain derived neurotrophic factor (BDNF) modulates neural plasticity, which has been implicated in Alzheimer's disease. We examined in cognitively normal older adults whether the BDNF codon 66 polymorphism affects β amyloid burden and the relationship betw...

The anti-amyloid β monoclonal antibody aducanumab was approved on June 7, 2021, by the US Food & Drug Administration (FDA) for treatment of Alzheimer's disease.1 Approval provided under FDA's accelerated approval process drugs that treat serious conditions and fill an unmet need, based surrogate endpoint reduction amyloid plaques in brain.

Unraveling the normal physiologic role of β-amyloid is likely crucial to understanding the pathogenesis of Alzheimer's disease. However, progress on this question is currently limited by the high background of many ELISAs for murine β-amyloid. Here, we examine the background signal of several murine β-amyloid ELISAs, and conclude that the majority of the background is from non-APP derived prote...

Senile plaques are mainly composed of different species of fibrillar β-amyloid (Aβ), a product of the cleavage of the β-amyloid precursor protein (APP), and they are surrounded by dystrophic neurites, reactive astrocytes and microglia. Aβ fibrillar deposits also occur in diffuse plaques, subpial deposits and in the wall of the cerebral and meningeal blood vessels in the form of amyloid angiopat...