Profiles

Maria Lindau

Universitetslektor, docent

Visa sidan på svenska
Works at Department of Psychology
Telephone 08-16 20 16
Email maria.lindau@psychology.su.se
Visiting address Frescati Hagväg 8
Room C 210
Postal address Psykologiska institutionen 106 91 Stockholm

Publications

A selection from Stockholm University publication database
  • 2016. Maria Lindau, Ove Almkvist, A. Mohammed. Stress, 153-159
  • 2014. Maria Lindau, R. Bjork. Dementia and Geriatric Cognitive Disorders 4 (3), 465-480

    Aims: To evaluate the occurrence of anosognosia (lack of awareness) and anosodiaphoria (insouciance) in mild cognitive impairment (MCI) and Alzheimer's disease (AD) and to evaluate the influence of a worsening of dementia on these phenomena. Methods: A self-evaluation scale was used assessing degrees of anosognosia and anosodiaphoria; furthermore, a neuropsychological assessment and statistical analyses with nonparametric tests which could cope with data on an ordinal scale level and small samples were employed. Results: Cognitive ability was lower in AD (n = 9) than in MCI patients (n = 12), but AD patients self-rated lower cognitive disabilities, which is interpreted as one relative sign of anosognosia in AD. Awareness of the reasons for cognitive problems was also lower in AD, which is considered as another sign of anosognosia. The main pattern in MCI found that the higher the awareness, the lower the cognitive ability. In AD low awareness paralleled low cognitive functioning. Anosodiaphoria was present in AD but not in MCI. Conclusion: According to the literature anosognosia and anosodiaphoria seem to increase with progression of dementia from MCI as a result of right hemispheric alterations.

  • 2013. M. Degerman Gunnarsson (et al.). Dementia and geriatric cognitive disorders extra 3 (1), 472-481

    Objectives: There is an overlap regarding Pittsburgh compound B (PIB) retention in patients clinically diagnosed as Alzheimer's disease (AD) and non-AD dementia. The aim of the present study was to investigate whether there are any differences between PIB-positive and PIB-negative patients in a mixed cohort of patients with neurodegenerative dementia of mild severity regarding neuropsychological test performance and regional cerebral glucose metabolism measured with [18F]fluoro-2-deoxy-d-glucose (FDG) positron emission tomography (PET). Methods: Eighteen patients clinically diagnosed as probable AD or frontotemporal dementia were examined with PIB PET, FDG PET and neuropsychological tests and followed for 5-9 years in a clinical setting. Results: The PIB-positive patients (7 out of 18) had slower psychomotor speed and more impaired visual episodic memory than the PIB-negative patients; otherwise performance did not differ between the groups. The initial clinical diagnoses were changed in one third of the patients (6 out of 18) during follow-up. Conclusions: The subtle differences in neuropsychological performance, the overlap of hypometabolic patterns and clinical features between AD and non-AD dementia highlight the need for amyloid biomarkers and a readiness to re-evaluate the initial diagnosis.

  • 2010. M. Degerman Gunnarsson (et al.). Dementia and Geriatric Cognitive Disorders 29 (3), 204-212

    Background: The positron emission tomography (PET) radiotracer Pittsburgh Compound-B (PIB) is an in vivo ligand for measuring β-amyloid (Aβ) load. Associations between PET PIB and cerebrospinal fluid (CSF) Aβ1–42 and apolipoprotein E ε4 (APOE ε4) have been observed in several studies, but the relations between PIB uptake and other biomarkers of Alzheimer’s disease (AD) are less investigated. Method: PET PIB, PET 18Fluoro-2-deoxy-D-glucose and different AD biomarkers were measured twice in CSF, plasma and urine 12 months apart in 10 patients with a clinical diagnosis of mild to moderate AD. Results: PIB retention was constant over 1 year, inversely related to low CSF Aβ1–42 (p = 0.01) and correlated positively to the numbers of the APOE ε4 allele (0, 1 or 2) (p = 0.02). There was a relation between mean PIB retention and CSF ApoE protein (r = –0.59, p = 0.07), and plasma cystatin C (r = –0.56, p = 0.09). Conclusion: PIB retention is strongly related to CSF Aβ1–42, and to the numbers of the APOE ε4 allele.

  • 2007. Christin Andersson (et al.). Dementia and Geriatric Cognitive Disorders 23 (2), 87-95

    Objectives: To investigate the relationships between episodic memory, APOE genotype, CSF markers (total tau, T-tau; phospho-tau, P-tau; beta-amyloid, A beta 42) and longitudinal cognitive decline. Methods: 124 memory clinic patients were retrospectively divided into 6 groups based on (i) episodic memory function (Rey Auditory Verbal Learning Test, RAVLT): severe, moderate or no impairment (SIM, MIM or NIM), and (ii) APOE genotype (epsilon 4+ or epsilon 4-). CSF marker levels and cognitive decline were compared across groups. Results: Episodic memory function, according to RAVLT scores, was significantly correlated with CSF marker levels only among epsilon 4+ subjects and not among epsilon 4- subjects. When comparing the 6 subgroups, SIM epsilon 4+ and MIM epsilon 4+ groups showed significantly lower A beta 42 levels than the other groups. T-tau and P- tau levels were significantly increased in SIM epsilon 4+ when compared to all the other groups, including the SIM epsilon 4- group. However, both SIM epsilon 4+ and SIM epsilon 4- declined cognitively during the follow-up. Conclusion: It remains to be determined whether APOE genotype affects the expression of biomarkers in CSF, or whether the different biomarker patterns reflect different types of disease processes in patients with progressive cognitive dysfunction. 

Show all publications by Maria Lindau at Stockholm University

Last updated: February 23, 2018

Bookmark and share Tell a friend