The Bio-imaging lab hosts several PhD students. For example The following PhD projects are currently running in the lab:
- Unraveling the effect of thyroid hormones on seasonal neuroplasticity in the song control system of adult songbirds - Funded by FWO
Prior studies mainly focused on the effect of T on SCS plasticity. However, it has been shown that steroid-independent photostimulation can also induce SCS plasticity, but its mechanism remains unclear. One of the proposed alternatives is the mediating effect of THs, as THs play an important role in the regulation of seasonal reproduction and are associated with neurogenesis. Surprisingly, the effect of THs on SCS plasticity has only been studied partially. In addition, it is unknown whether THs mediate SCS plasticity in a direct or an indirect manner.
- Spatial neglect in rodents: a model for studying neuroplasticity at the network level - Funded by BOF
Diseases that afflict the brain, such as stroke, are associated with high morbidity for patients and their families and incur a tremendous burden to individuals and the society. Spatial neglect is a frequent consequence of brain damage, manifesting attentional deficits in perceiving and responding to stimuli in the contralesional field. Neglect affects roughly one third of stroke victims and greatly interferes with all daily activities, being one of the most disabling neurological syndromes. Despite partial recovery in the first months after stroke, yet poorly understood, one third of these patients remain severely disabled and require specific treatment. Although a number of treatments exist for human patients none is extremely successful, as we do not understand sufficiently the neural mechanisms underlying the disorder with multiple questions remaining to be addressed. To tackle some of these complicated issues, we propose to use a multimodal approach that combines functional magnetic resonance imaging, electrophysiology and stimulation of neuromodulatory nuclei in a rat model of spatial neglect.
- How the interplay between basal forebrain neuronal populations determines brain state and how this is changed in Alzheimer's disease. - Funded by BOF
During the last decades, the achievement of a better and improved quality of life has resulted in increased life expectancy. This is mainly due to progress in translational research and development of new therapeutic approaches. The downside is that age is one of the major risk factors for dementias and neurodegenerative disorders such as Alzheimer's disease (AD), characterized by a marked decline of cognitive functions (e.g. short- and long-term memory loss) and dysregulation of higher cortical functions (e.g. impaired judgement and thinking). The pathological condition of these diseases is disabling enough to compromise the activity of everyday life. Lengthening the life span has little value if the quality of life cannot be ensured. Unfortunately, the pathogenesis of AD is still far from being understood and this could be the reason why none of the currently available pharmacological therapies for this disease are satisfactory. Current treatments are purely symptomatic and do not act on the onset and progression of the pathology. It is well known that Basal Forebrain (BF) cholinergic neurons are prone to degeneration during aging as well as in dementias like AD. Furthermore, "the cholinergic hypothesis of geriatric cognitive dysfunction" is also supported by the significant correlation between the level of cholinergic depletion and the degree of cognitive deficits. Acetylcholine is a neuromodulator broadly investigated for its role in learning and memory, but it is not the only player in AD. In fact, in the BF, intermingled with cholinergic neurons, there are also two non-cholinergic neuronal types: GABAergic and glutamatergic neurons. It has been discovered that dysfunctions at the level of glutamatergic and GABAergic systems are involved as well in AD. Until recently, neuroscientists have limited the research of AD to the study of a single neuronal type (mainly BF cholinergic neurons), overlooking the possible role of non-cholinergic neuronal populations (GABAergic and glutamatergic). However, it is of the utmost importance to uncover the interaction between BF cholinergic and non-cholinergic neurons to develop novel strategies for the treatment of AD. The proposed research project aims to investigate the interaction between the three distinct BF populations and to elucidate how the BF cholinergic neuronal activity influences the other two BF neuronal types both in healthy and in pathological conditions.