Topic: APP/PS1

Understanding the cellular mechanisms underlying learning and their alteration in Alzheimer’s disease (AD) is crucial for developing targeted therapies. We aimed to elucidate coordinated astrocytic and neuronal activities in learning, with a specific focus on their dynamics influenced by experience and alterations in AD. Using calcium imaging of neurons and astrocytes in the APP/PS1 double transgenic Alzheimer’s disease mouse model, we investigated behavioural and cellular responses to repetitive visual stimuli, in comparison with littermate wild type (WT) mice.We collected data from 32 female

Studies have shown that ergothioneine (ergo), a derivative of histidine synthesized by certain fungi and actinobacteria, can protect against neuronal injury induced by exogenous Aβ. Our aim is to investigate the role of ergo in synaptic plasticity using the AD mouse model. Field electrophysiology was performed in the CA1 region of hippocampal slices from male C57BL/6 mice to measure synaptic modification over time. Hippocampal slices from the double transgenic AD mouse model APP/PS1, when stimulated with a strong tetanisation protocol, exhibit impaired late long-term potentiation (late-LTP), w

Heat shock proteins (HSPs) are evolutionarily conserved chaperones. Previously our group observed that overexpression of HSPB1 improved certain symptoms of Alzheimer’s disease (AD) in mice. The primary role of these chaperons is to maintain the protein homeostasis, however, several evidence suggest that they have additional functions, such as regulating inflammation. Therefore, our aim is to investigate the role of HSPB1 in chronic neuroinflammation and glia activation in a mouse model of AD.AD model (APP/PS1) mouse strain was crossed with an HSPB1 overexpressing line. Expression pattern of HS

Spatial navigation impairments are among the earliest clinical manifestations of Alzheimer’s Disease (AD). Pyramidal cells of the hippocampus fire selectively when the animal is in a specific location in the environment, leading to the theory that the hippocampus plays a crucial role in forming a cognitive map of the environment. The phenomenon of “remapping”, where specific cells exhibit selective firing in distinct environments, is thought to support the formation of different memories. By performing in-vivo electrophysiological recordings in freely moving mice while they navigate through di

Obesity is linked to neurodegenerative diseases through neuroinflammation. Pleiotrophin (PTN) is a cytokine that is upregulated in different neuroinflammatory disorders of diverse origin. PTN is a ligand and an endogenous inhibitor of Receptor Protein Tyrosine Phosphatase (RPTP) β/ζ. To investigate the role of RPTP β/ζ, in neuroinflammation and neurodegeneration, we used the APP/PS1 genetic model of Alzheimer disease (AD) and a high-fat diet (HFD)-induced obesity model. Three-month-old wild type (WT) mice were fed with standard chow or HFD (60 Kcal % fat) for three months. MY10, an exogenous R

Aging produces in brain a progressive oxidative process and neuroinflammation that deteriorates cognition. These brain dysfunctions provoke high economic and social costs to developed societies. For this reason, the search for treatments to prevent cognitive deficits associated with aging is a priority. Previous results suggest that STX64, a steroid sulfatase (STS) inhibitor, improves cognition in neurodegenerative diseases. In this work, we have designed cellular (immunohistochemistry), molecular (qPCRs with primers of inflammatory markers and cellular populations) and behaviour (mainly, obje

The retina, as part of the central nervous system, shows abnormalities in Alzheimer`s disease (AD) and type 2 diabetes (T2D). Importantly, analysis of the retina may provide a non-invasive approach with diagnostic and prognostic value for cognitive decline. In addition, T2D increases risk to suffer AD. Accordingly, we have analyzed structural and functional alterations, by spectral domain optical coherence tomography and electroretinography (ERG) respectively, in the retina from APP/PS1 (AD model), db/db (T2D model) and APP/PS1xdb/db (AD-T2D model) animals at 4 weeks of age, before the onset o

Alzheimer's disease (AD) is the most common form of dementia after the age of 65. Prior to cognitive impairment, this disease is characterized by a long asymptomatic phase during which dysfunctions of neurotransmission have been demonstrated. It is known that these early dysfunctions are the result of an abnormal accumulation of β-amyloid peptide which accumulates in different regions of the brain, notably the hippocampus. By performing electrophysiological recordings on the APP/PS1 transgenic mouse model that show an overproduction of β-amyloid peptide, I identified an alteration of the inhib

Understanding the neural mechanisms underlying memory formation and retrieval is fundamental to unraveling the pathophysiology of Alzheimer's disease (AD). Inhibitory interneurons have fundamental roles in shaping neural circuits and synaptic plasticity within the hippocampus, a brain region critical for memory encoding and consolidation. However, the specific contribution of inhibitory interneurons to the formation and maintenance of engrams, the neural representations of memories, remains poorly understood, particularly in the context of AD.To determine neurons participating in the engram fo

Alzheimer’s disease (AD) is the most common cause of dementia. Despite age being the main risk factor, previous studies have also reported that type 1 diabetes (T1D) may contribute to abnormal tau phosphorylation and worsen cognitive impairment in AD patients. However, the underlying mechanisms are not completely understood. Therefore, we have analyzed the effects of streptozotocin (STZ)-induced T1D in a mouse model of AD (APP/PS1) in terms of metabolic impairment, cortical tau phosphorylation and cognition at 26 weeks of age, when the pathology is fully established. When all groups under stud