New and Noteworthy Information—April 2014
For patients with Alzheimer’s disease, levels of markers of neuronal injury in the spinal fluid may decrease as symptoms of memory loss and mental decline appear, according to research published March 5 in Science Translational Medicine. Investigators studied data from the Dominantly Inherited Alzheimer’s Network, which includes participants from families with genetic mutations that cause rare inherited forms of Alzheimer’s disease. The group examined levels of tau, p-tau, and visinin-like protein-1 (VILIP-1). Asymptomatic mutation carriers had elevated concentrations of CSF tau, p-tau181, and VILIP-1 10 to 20 years before their estimated age at symptom onset and before cognitive deficits were detected. The concentrations of CSF biomarkers of neuronal injury or death decreased after their estimated age at symptom onset, suggesting a slowing of acute neurodegenerative processes with symptomatic disease progression.
Men with poor cardiovascular fitness or a low IQ at age 18 are more likely to develop dementia before age 60, investigators reported online ahead of print March 6 in Brain. The researchers conducted a population-based cohort study of more than 1.1 million Swedish male conscripts (age 18) who underwent conscription exams between 1968 and 2005. Participants were followed for as long as 42 years. In fully adjusted models, low cardiovascular fitness and cognitive performance at age 18 were associated with increased risk for future early-onset dementia and mild cognitive impairment, compared with high cardiovascular fitness and cognitive performance. Poor performance on cardiovascular fitness and cognitive tests was associated with a greater-than-sevenfold and a greater than eightfold increased risk of early-onset dementia and early-onset mild cognitive impairment, respectively.
A test that detects low levels of prion protein in the blood may accurately screen for infection with the agent responsible for variant Creutzfeldt-Jakob disease (vCJD), according to a study published online ahead of print March 3 in JAMA Neurology. Researchers performed the test on samples from national blood collection and prion disease centers in the US and the UK. The samples were taken from healthy donors, patients with nonprion neurodegenerative disease, patients in whom a prion disease diagnosis was likely, and patients with confirmed vCJD. The assay’s specificity was confirmed as 100% in a healthy UK cohort. No potentially cross-reactive blood samples from patients with nonprion neurodegenerative diseases tested positive. Two patients with sporadic CJD tested positive. The authors’ previous sensitivity estimate was reconfirmed but not refined.
The FDA has approved Neuraceq (florbetaben F18 injection) for PET imaging of the brain to estimate beta-amyloid neuritic plaque density in adults with cognitive impairment who are being evaluated for Alzheimer’s disease and other causes of cognitive decline. The approval is based on safety data from 872 patients who participated in global clinical trials, and on three studies that examined images from adults with a range of cognitive function. Images were analyzed from 82 subjects with postmortem confirmation of the presence or absence of beta-amyloid neuritic plaques. Correlation of the visual PET interpretation with histopathology in these 82 brains demonstrated that Neuraceq (Piramal Imaging; Boston) accurately detects moderate to frequent beta-amyloid neuritic plaques in the brain.
A combination of human umbilical cord blood cells (hUCBs) and granulocyte colony stimulating factor (G-CSF) may provide more benefit for patients with traumatic brain injury (TBI) than either therapy alone, according to research published March 12 in PLOS One. Adult rats underwent moderate TBI and, seven days later, were treated with saline alone, G-CSF and saline, hUCB and saline, or hUCB and G-CSF. The rats treated with saline exhibited widespread neuroinflammation, impaired endogenous neurogenesis, and severe hippocampal cell loss. hUCB monotherapy suppressed neuroinflammation, nearly normalized neurogenesis, and reduced hippocampal cell loss, compared with saline alone. G-CSF monotherapy produced partial and short-lived benefits characterized by low levels of neuroinflammation, modest neurogenesis, and moderate reduction of hippocampal cell loss. Combined therapy robustly dampened neuroinflammation, enhanced endogenous neurogenesis, and reduced hippocampal cell loss.
The ability to learn new information may be significantly poorer among patients with Parkinson’s disease than among healthy individuals, according to research published online ahead of print February 24 in Movement Disorders. Investigators examined 27 patients with Parkinson’s disease without dementia and 27 age-, gender-, and education-matched healthy controls with a neuropsychologic test battery designed to assess new learning and memory. The researchers found a significant difference in the groups’ ability to learn a list of 10 semantically related words. Once the groups were equated on learning abilities, the investigators found no significant difference between patients with Parkinson’s disease and controls in recall or recognition of the newly learned material. The memory deficit in nondemented patients with Parkinson’s disease largely results from a deficit in learning new information, said the authors.
