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Replies to post #190373 on Anavex Life Sciences Corp (AVXL)
04/25/19 4:58 AM
"Preparatory work is ongoing at Sahlgrenska University Hospital in Gothenburg to make this method available as a clinical procedure in the near future. Physicians can then use the method to measure damage to nerve cells in Alzheimer's disease and other brain disorders through a simple blood test," Mattsson concludes.
Western blotting verified the direction and magnitude of change for severdal proteins in different subcellular fractions as follows: neurofilament light protein (NEFL) and 2',3'-cyclic-nucleotide 3'-phosphodiesterase (CNP) in the total homogenate; heterogeneous nuclear ribonucleoproteins C1/C2 (HNRNPC) and heterogeneous nuclear ribonucleoprotein D0 (HNRNPD) in the nuclear fraction; excitatory amino acid transporter 2 (EAAT2) and ras-related protein rab 3a (RAB3A) in the synaptic fraction; and ras-related protein rab 35 (RAB35) and neuromodulin (GAP43) in the rough endoplasmic reticulum fraction.
Differential effects of neurodegeneration biomarkers on subclinical cognitive decline.
Merluzzi AP1, Vogt NM1, Norton D2, Jonaitis E2, Clark LR1,3, Carlsson CM1,3, Johnson SC1,3, Asthana S1,3, Blennow K4,5, Zetterberg H4,5,6,7, Bendlin BB1.
Author information
1
Wisconsin Alzheimer's Disease Research Center, University of Wisconsin-Madison, Madison, WI, USA.
2
Department of Biostatistics and Medical Informatics, University of Wisconsin-Madison, Madison, WI, USA.
3
Geriatric Research Education and Clinical Center, William S. Middleton Memorial Veteran's Hospital, Madison, WI, USA.
4
Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
5
Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.
6
Institute of Neurology, University College London, Queen Square, London, UK.
7
UK Dementia Research Institute, London, UK.
Abstract
INTRODUCTION:
Neurodegeneration appears to be the biological mechanism most proximate to cognitive decline in Alzheimer's disease. We test whether t-tau and alternative biomarkers of neurodegeneration-neurogranin and neurofilament light protein (NFL)-add value in predicting subclinical cognitive decline.
METHODS:
One hundred fifty cognitively unimpaired participants received a lumbar puncture for cerebrospinal fluid and at least two neuropsychological examinations (mean age at first visit = 59.3 ± 6.3 years; 67% female). Linear mixed effects models were used with cognitive composite scores as outcomes. Neurodegeneration interactions terms were the primary predictors of interest: age × NFL or age × neurogranin or age × t-tau. Models were compared using likelihood ratio tests.
RESULTS:
Age × NFL accounted for a significant amount of variation in longitudinal change on preclinical Alzheimer's cognitive composite scores, memory composite scores, and learning scores, whereas age × neurogranin and age × t-tau did not.
DISCUSSION:
These data suggest that NFL may be more sensitive to subclinical cognitive decline compared to other proposed biomarkers for neurodegeneration.
