Topic: Aβ

Microglial phenotype during Alzheimer’s Disease (AD) continuum is under debate. At early stages, a protective phenotype with the typical DAM profile would participate in plaque compaction and Aβ degradation. Instead, human AD microglia (HAM) show an enhance aged/degenerative profile, supporting a microglial dysfunction as a central mechanism in AD aetiology. Recent findings from our lab described that peri-plaque microglia are highly reliant on oxygen levels and mitochondrial integrity. Nevertheless, mitochondrial implication in aged microglia during the disease progression remains unclear. Th

Alzheimer Disease’s (AD) etiology is a hot topic in neuroscience. Cholinergic hypothesis was the earliest theory while amyloidogenic hypothesis is currently the most studied. Unfortunately, despite massive and prolonged efforts, triggering events responsible for AD genesis remain elusive. Here, we aim to elucidate the cellular and molecular mechanisms that induce AD by focusing on glutamatergic tripartite synapses in hippocampus. It is known that Aβ binds to α7 Acetylcholine nicotinic receptors (α7nAchRs) with high affinity, favoring synaptic plasticity at physiological picomolar concentration

Alzheimer's disease (AD) is the most prevalent neurodegenerative disorder, characterized by the accumulation of Aβ and Tau proteins. While many animal models primarily focus on Aβ, this study centers on characterizing a tauopathy model, the PS19 model (B6;C3-Tg(Prnp-MAPT*P301S)PS19Vle/J), to explore the pathological role of tau in AD.36 PS19 and 24 non-carrier mice (NCAR) were followed from 12 to 50 weeks, assessing locomotor, behavior, and memory activity, neurodegeneration, neuroinflammation, blood-brain barrier (BBB) integrity, cerebral glucose metabolism, and neurodegenerative progression

The delivery of molecules like galantamine and DNA aptamers to the brain for the treatment of neurodegenerative diseases is a great challenge because of the blood-brain barrier selectivity. However, nanoliposomal systems can provide an alternative to this drawback. This study aimed to design and develop nanoliposomes based on soy lecithin loaded with galantamine (acetylcholinesterase inhibitor) or DNA aptamers designed to hinder the aggregation of proteins like Aβ, TDP-43 and α-synuclein. For this, a complete physicochemical characterization of soy lecithin and other raw materials was carried

Neurodegenerative diseases like Alzheimer’s disease and Progressive Supranuclear Palsy (PSP) exhibit synaptic loss. In these conditions, synaptic loss precedes neuronal degeneration, and the degree of synaptic loss correlates closely with the severity of clinical symptoms. Both Aβ, which accumulates in amyloid plaques in AD, and tau protein which accumulates intracellularly in tauopathies, accumulate within synaptic terminals. In model systems, the accumulation of Aβ and tau in synapses has been linked to synaptic dysfunction, synaptic loss, and the spread of pathology trans-synaptically. Howe

Alzheimer's Disease (AD) are characterized with the accumulation of hyperphosphorylated tau protein and Aβ and neuroinflammation. Disrupted myelin has been observed in the brains of AD patients before the onset of symptoms. However, it remains unknown the function of myelin-forming cells in AD pathogenesis. Oligodendrocyte precursor cells (OPCs) are the source cells of myelin-forming cells in the central nervous system (CNS). In this study, we observe an abnormally enhanced microglial phagocytosis upon in activation of autophagy in OPCs. AD transgenic mice harboring defective autophagy exhibit

Aβ plays an important role in the pathogenesis of Alzheimer’s disease (AD), and passive immunotherapy targeting Aβ has emerged as a promising treatment approach. However, the administration of antibody drugs is limited due to many concerns. Therefore, using adeno-associated virus (AAV) gene therapy to deliver antibody drugs may introduce innovative treatment regimens for AD. We have previously shown that NP106, a novel anti-Aβ antibody, exhibits multiple therapeutic benefits for ameliorating brain Aβ burden and cognitive impairment in APP/PS1 mouse model of AD. In this study, we developed an N