Neuronal A2A Receptor Exacerbates Synapse Loss and Memory Deficits in APP/PS1 Mice

A2A Adenosine Receptor Exacerbates Synaptic Loss and Memory Deficits in APP/PS1 Mice Alzheimer’s disease (AD) is a neurodegenerative disorder associated with progressive cognitive decline, characterized by the deposition of extracellular β-amyloid (Aβ) plaques and the accumulation of hyperphosphorylated tau protein in neurons. Some epidemiological ...

Diurnal Characteristics of the Orexin System Genes and Its Effects on Pathology at Early Stage in 3XTg-AD Mice

Study on the Circadian Rhythm of Orexin System Genes and Their Impact on Early Alzheimer’s Disease (AD) Pathology Research Background and Objectives Alzheimer’s Disease (AD) is a chronic degenerative disease of the central nervous system, characterized by senile plaques formed by β-amyloid protein (Aβ) aggregation and neurofibrillary tangles formed...

Probable Novel APP Met671Leu Mutation in a Chinese Han Family with Early-Onset Alzheimer’s Disease

A Study Exploring a New Mutation in Early-Onset Alzheimer’s Disease Alzheimer’s Disease (AD) is a common neurodegenerative disorder, accounting for 60-70% of all dementia cases. In recent years, with global population aging and environmental changes, the incidence of AD has been increasing annually. It is predicted that by 2050, the number of patie...

Aβ-Aggregation-Generated Blue Autofluorescence Illuminates Senile Plaques as Well as Complex Blood and Vascular Pathologies in Alzheimer’s Disease

Blue Autofluorescence Generated by Aβ Aggregation Illuminates Senile Plaques and Complex Blood and Vascular Pathologies in Alzheimer’s Disease Research Background Alzheimer’s disease (AD) is a widespread neurodegenerative disorder globally, with senile plaques being the main pathological hallmark of AD, primarily composed of β-amyloid protein (Aβ)....

Low-dose IL-2 treatment rescues cognitive deficits by repairing the imbalance between Treg and Th17 cells at the middle Alzheimer's disease stage

Low-dose IL-2 treatment rescues cognitive deficits by repairing the imbalance between Treg and Th17 cells at the middle Alzheimer’s disease stage Background Alzheimer’s disease (AD) is an age-related neurodegenerative disorder characterized by neuronal damage, amyloid plaque deposition, and chronic inflammation in the central nervous system (CNS). ...