About the project
The development of dementia involves a neurological process which progresses over many years from normal functioning to mild cognitive difficulties and further to dementia. Mild cognitive impairment can have many causes, and the project aims to identify risk factors which are associated with dementia development. Patients at AHUS (Akershus University Hospital) with mild cognitive impairment shall be investigated with cognitive tests, MR-scanning of the brain and other bio-markers. Follow up over time will give a foundation for the identification of risk factors.
Objectives
The objective is to treat dementia disorders at an early stage and thereby delay or stop the development of dementia.
Outcomes
We have studied how a combination of MR changes in brain areas of significance for memory, in combination with pathological markers in spinal fluid, affect neuropsychological function. In addition to signs of atrophy of the hippocampus, MR measurements also suggest a weakened integrity of fibre connections to other areas have significance for cognitive functions. The group with abnormal total tau in the spinal fluid strings had more serious memory loss and hippocampal atrophy, while those with normal total tau had weakened fibre integrity. See publications.
Background
The project is cooperation with the University of Gothenburg and covers a broad spectrum of cognitive, neurological, biological and genetic factors. It build on an hypothesis on mechanism and chronology in development of Alzheimer’s disease which demands a multifactorial approach and a long term follow up period for testing. A common investigation protocol will facilitate faster results.
Sub-projects
The Centre for Study of Human Cognition is responsible for the charting of cognitive function in the Norwegian part of the survey. One hypothesis is that different types of cognitive dysfunction are associated with different biomarkers and different prognosis. We have shown that patients with memory loss differ from patients with impairment of other cognitive functions on MR.
Publications
Stenset V, Grambaite R, Reinvang I, Hessen E, Cappelen T, Bjornerud A, Gjerstad L, Fladby T. (2007) Diaschisis after thalamic stroke: a comparison of metabolic and structural changes in a patient with amnesic syndrome. Acta Neurol Scand Suppl., 187, 68-71
Stenset V, Hofoss D, Johnsen L, Skinningsrud A, Berstad AE, Negaard A, Reinvang I, Gjerstad L, Fladby T. (2008) White matter lesion severity is associated with reduced cognitive performances in patients with normal CSF Abeta42 levels.Acta Neurol Scand. ;118(6):373-8.
Fjell AM, Walhovd KB, Amlien I, Bjørnerud A, Reinvang I, Gjerstad L, Cappelen T, Willoch F, Due-Tønnessen P, Grambaite R, Skinningsrud A, Stenset V, Fladby T. (2008) Morphometric changes in the episodic memory network and tau pathologic features correlate with memory performance in patients with mild cognitive impairment. AJNR Am J Neuroradiol.29(6):1183-9.
Grambaite R, Stenset V, Reinvang I, Walhovd KB, Fjell AM, Fladby T. (2009). White matter diffusivity predicts memory in patients with subjective and mild cognitive impairment and normal CSF total tau levels. J Int Neuropsychol Soc. 2009, 19:1-12.
Walhovd KB, Fjell AM, Amlien I, Grambaite R, Stenset V, Bjørnerud A, Reinvang I, Gjerstad L, Cappelen T, Due-Tønnessen P, Fladby T. (2009). Multimodal imaging in mild cognitive impairment: Metabolism, morphometry and diffusion of the temporal-parietal memory network. Neuroimage, 45(1):21
Thorvaldsson V, Nordlund A, Reinvang I, Blennow K, Zetterberg H, Wallin A, Johansson B. (2010). Memory in individuals with mild cognitive impairment in relation to APOE and CSF Abeta42. Int Psychogeriatr. 22(4):598-606.
