Back to Authors

Minthon, Lennart

A5080476940 | I4210137844

Mayo Clinic

Skåne University Hospital

Citations 4

P1‐139: THE CONTRIBUTION OF SEX‐SPECIFIC ASSOCIATIONS IN GENETIC STUDIES OF ALZHEIMER'S DISEASE PATHOLOGY

Alzheimer's & Dementia | October 22, 2018 | Volume: 14 | Issue: 7S_Part_6 | Pages: No page available

10.1016/j.jalz.2018.06.142

Low Levels of Soluble NG2 in Cerebrospinal Fluid from Patients with Dementia with Lewy Bodies

Journal of Alzheimer's Disease | June 4, 2018 | Volume: 40 | Issue: 2 | Pages: 343-350

10.3233/jad-132246 | PMID 24448788

O2‐10‐05: Cerebrospinal Fluid Levels of Amyloid Beta and Tau as Endophenotypes Reveal Novel Variants Potentially Informative for Alzheimer's Disease

Alzheimer's & Dementia | October 17, 2016 | Volume: 12 | Issue: 7S_Part_5 | Pages: No page available

10.1016/j.jalz.2016.06.452

Kynurenic Acid Levels in Cerebrospinal Fluid from Patients with Alzheimer's Disease or Dementia with Lewy Bodies

International Journal of Tryptophan Research | April 28, 2014 | Volume: 7 | Issue: No issue available | Pages: No page available

10.4137/ijtr.s13958 | PMID 24855376

Kynurenic acid (KYNA) is implicated in cognitive functions. Altered concentrations of the compound are found in serum and cerebrospinal fluid (CSF) of patients with Alzheimer's disease (AD). Further studies to determine whether KYNA serves as a biomarker for cognitive decline and dementia progression are required. In this study, we measured CSF KYNA levels in AD patients (n = 19), patients with dementia with Lewy bodies (DLB) (n = 18), and healthy age-matched controls (Ctrls)) (n = 20) to further explore possible correlations between KYNA levels, cognitive decline, and well-established AD and inflammatory markers. Neither DLB patients nor AD patients showed significantly altered CSF KYNA levels compared to Ctrls. However, female AD patients displayed significantly higher KYNA levels compared to male AD patients, a gender difference not seen in the Ctrl or DLB group. Levels of KYNA significantly correlated with the AD-biomarker P-tau and the inflammation marker soluble intercellular adhesion molecule-1 (sICAM-1) in the AD patient group. No associations between KYNA and cognitive functions were found. Our study shows that, although KYNA was not associated with cognitive decline in AD or DLB patients, it may be implicated in AD-related hyperphosphorylation of tau and inflammation. Further studies on larger patient cohorts are required to understand the potential role of KYNA in AD and DLB.