https://www.um.edu.mt/library/oar/handle/123456789/940 Mon, 13 Apr 2026 03:35:29 GMT 2026-04-13T03:35:29Z https://www.um.edu.mt/library/oar/handle/123456789/1097 Title: Effects of nicotine administration on amyloid precursor protein metabolism, neural cell genesis and acquisition of spatial memory Authors: Scerri, Charles Abstract: Nicotine is reported to improve learning and memory in experimental animals. Improved learning and memory has also been related to increased neural cell genesis in the dentate gyrus of the brain hippocampal formation. Stimulation of acetylcholine receptors has also been found to enhance the expression and secretion of amyloid precursor protein (APP) in various cell lines. Aberrent metabolism of APP generates amyloid-beta (Abeta) peptide which is the major pathological lesion found in the brains of Alzheimer’s disease (AD) patients. This paper will focus on the the results obtained in our laboratory on the effects of acute and chronic nicotine administration on the metabolism of APP, its role in spatial learning and neural cell genesis in the rat brain. Sat, 01 Jan 2011 00:00:00 GMT https://www.um.edu.mt/library/oar/handle/123456789/1097 2011-01-01T00:00:00Z https://www.um.edu.mt/library/oar/handle/123456789/1096 Title: Sources of extracellular glutamate in developing white matter Authors: Fern, Robert Abstract: Neurotransmitters mediate synaptic communication between neurons and are therefore fundamental to such essential human characteristics as learning, memory, cognition and persona. Recent work indicates that neurotransmitters and their receptors are also used for communication between non-synaptic elements of the nervous system and may be involved in glial-glial, glia-axon and glial-neuronal information transfer and processing. We have recently found evidence that glial cells in developing white matter, which contains no synapses or neuronal somata, express a wide variety of neurotransmitter receptors, including the NMDA-type glutamate receptor that had long thought to be exclusively neuronal. At the point when white matter is laying down myelin and glial cells are forming their long-term morphological arrangement with axons, NMDA receptors mediate post-synaptic-potential input onto glia and may be crucially involved in stabilizing glial-axonal cyto-architecture. There is also strong evidence that glutamate receptors on glial cell membranes greatly heighten the cells susceptibility to injury, a phenomenon that may explain the selective damage of developing white matter found in common human birth disorders such as cerebral palsy. There are many potential sources of extracellular glutamate in ischemic white matter including axons, oligodendrocytes, reverse glutamate transport, loss of astrocyte processes and astrocyte swelling. These potential pathways for glutamate release are described here. Sat, 01 Jan 2011 00:00:00 GMT https://www.um.edu.mt/library/oar/handle/123456789/1096 2011-01-01T00:00:00Z https://www.um.edu.mt/library/oar/handle/123456789/1095 Title: Understanding the Pathogenesis of Neuroinflammation using Magnetic Resonance Imaging Authors: Waiczies, Sonia; Waiczies, Helmar Abstract: A non-invasive view of the brain with the aid of magnetic resonance imaging (MRI) is invaluable for studying pathological processes during autoimmune encephalomyelitis. Several MRI technologies are available that can be employed to study inflammation within the brain. These include labeling of inflammatory cells with paramagnetic contrast agents (such as USPIO/SPIO/VSOP iron-oxide or perfluoro carbon (PFC)-rich nanoparticles) and new tools that facilitate high resolution imaging particularly MR microscopy (µMRI, microscopic MRI; MR histology). In this review we will go into both MRI technologies, with a special focus on their applicability in studying brain inflammation in the experimental autoimmune encephalomyelitis (EAE). Regarding cell labeling we will focus on PFC nanoparticles and fluorine (19F) MRI since these have introduced a number of advantages over T2*-weighted MRI with paramagnetic iron-oxide nanoparticles. Another MRI technology that we will be discussing is high resolution µMRI with cryogenically-cooled RF coils. This technology will enable neuroscientists to achieve a comprehensive, detailed and non-invasive view of the brain within short acquisition times: an important practical consideration when conducting longitudinal studies on the kinetics and dynamics of immune cell infiltration into the brain. Sat, 01 Jan 2011 00:00:00 GMT https://www.um.edu.mt/library/oar/handle/123456789/1095 2011-01-01T00:00:00Z https://www.um.edu.mt/library/oar/handle/123456789/1094 Title: The potential role of dietary polyphenols in Parkinson’s disease Authors: Caruana Grech Perry, Mario; Vassallo, Neville Abstract: Cumulative evidence now suggests that the abnormal aggregation of the neuronal protein alpha-synuclein is critically involved in the pathogenesis of synucleinopathies, of which Parkinson’s disease (PD) is the most prevalent. Development of neuropathology appears to be linked to events that accelerate the rate of aggregation of alpha-synuclein from monomers, via soluble oligomeric intermediates, into amyloid fibrils. Although increasing data suggest that oligomeric aggregates, not amyloid fibrils, disrupt or permeabilise cellular membranes, the nature of the neurotoxic species and its precise molecular mechanism still remain largely unknown, hampering the development of an effective treatment for the disease. Currently, there is no approved therapeutic agent directed toward preventing alpha-synuclein aggregation and only symptomatic therapies are available with a limited time-frame of utility. Numerous studies have demonstrated the protective effects of dietary polyphenols against neuronal damage in PD. The aim of this review is to look at what research has been done so far to show that dietary polyphenolic compounds can effectively interfere with alpha-synuclein oligomerisation. Evidence in the role and mechanisms of diet-derived phenolic products may guide the design of novel therapeutic drugs that can block early stages of amyloid self-assembly in PD and related synucleinopathies. Sat, 01 Jan 2011 00:00:00 GMT https://www.um.edu.mt/library/oar/handle/123456789/1094 2011-01-01T00:00:00Z