Topic: amyloid precursor protein

Numerous studies have shown the involvement of Traumatic Brain Injury (TBI) in increasing the risk of developing dementia and Alzheimer’s Disease (AD) with age, yet the intricate details of how TBI could increase the risk of such afflictions remain obscure. The scarcity of research in this area can be attributed partially to the lack of suitable animal models that can carry humanized versions of the genes known to pose a risk for developing AD. We used two cohorts of 6 months old mice, each consisting of 10 animals (5 males), carrying humanized versions of Amyloid Precursor Protein (APP), Tau

Alzheimer’s disease (AD) has wide-ranging health and economical impact affecting millions globally. The molecular mechanisms behind AD are not yet understood, but alterations in the processing and clearance of Amyloid precursor protein (APP), such as increased levels of specific APP fragments like Amyloid-ß peptide (Aß), have been observed in early-stage AD. Increased Aß concentration leads to impaired long-term potentiation (LTP) at hippocampal CA1-CA3 synapses, the process that can be restored by partially blocking GluN2B-NMDA receptor (Ronicke et al., Neurobiol. Aging 2011). We modeled comp

Oligodendrocytes, the myelinating glial cells of the central nervous system (CNS), surround axons with their membrane extensions, forming the myelin sheath. Loss of oligodendrocytes and/or myelin (demyelination) occurs in traumatic brain injury or pathologies such as multiple sclerosis. Since, there is no specific treatment for demyelination; we are interested in enhancing myelin endogenous repair. We focus our work on A Disintegrin and Metalloprotease (ADAM) 10, the major CNS α-secretase, which generates the neuroprotective soluble fragment sAPPα via cleavage of the Amyloid Precursor Protein

The full-length amyloid precursor protein (APP), a key player in Alzheimer’s disease (AD), is ubiquitously expressed in a large majority of neurons, including GABAergic interneurons (INTs). Recent studies showed evidence of disrupted hippocampal plasticity in conditional APP KO of GABAergic forebrain neurons (Mehr et al, 2020). However, the physiological functions of APP at inhibitory synapses remain to be defined. We to study the role of APP at inhibitory synapses onto CA3 pyramidal cells (PCs) as well as on the overall inhibitory balance within the CA3 network. We combine slice electrophysio

Alzheimer’s disease (AD) is characterised by the aberrant aggregation of two proteins within the brain- amyloid-β which deposits in extracellular plaques and the tau protein which forms neurofibrillary tangles. However, it is tau spreading that best correlates with clinical symptoms in AD, whilst the mechanisms that potentially drive tau spreading remain still unknown. More recently a study has demonstrated that binding of tau fibrils to the extracellular region of the Amyloid Precursor Protein (APP) led to the uptake of tau into cells, suggesting that APP may function as a tau fibril receptor

Synapse loss is a key feature of cognitive decline in Alzheimer’s disease (AD). Emerging evidence points toward the involvement of glial cells, alongside neurons, in disease progression. Understanding how glia remodel synaptic connections is crucial for understanding the onset of AD. Additionally, in the context of AD-specific risk genes, how this intricate balance is disrupted will aid in deciphering early disease mechanisms. In this study, primary glia cells were co-cultured in 3D with primary neurons pre-treated with pharmacological modulators targeting amyloid precursor protein (APP) proce