From my perspective, one of the most troublesome problems of the human species blocking the next evolutionary leap is the apparent reduction in empathy, compassion and the ability to "put oneself
in another's shoes."
During the past decade, the discovery of the "controversial" mirror-neurons in chimps, the potential of non-invasive, magnetic brain stimulation, and the promise of empathy- enhancing substances such as oxytocin appear to be encouraging breakthroughs.
However, despite these and other physiological advances, the growing stress
of living in a dangerously competitive world continues to ignite the
flames of fear-based aggression among nations, cultures, races,
businesses, families, groups and individuals.
Moreover, I find it difficult to ignore the willful, self-serving fanning
of those flames by powerful governments, industries, politicians and corporations and individuals who profit in many ways from the fear of difference that
seems to be rampant on the planet.
Consequently, my wish for the next advance in brain research would be the
development of methods to permit populations to scientifically evaluate
the brains of candidates before electing them to powerful positions of
authority.
In such a brave, new world, strength of leadership might include such
characteristics as better control of impulsivity, a capacity to tolerate
and understand the complexity of reality without false simplifications,
better deductive reasoning and higher quality decision-making abilities.
And although "even paranoids may have real enemies," leaders should possess an enhanced capacity for actual empathy and
compassion as well as an ability to quickly analyze risk and act decisively when necessary.
And while I'm dreaming, I should recommend development of a Gross National Happiness statistic to be added to the material indices we watch
so carefully. It might produce data with which we could really evaluate the value of our leaders.
Longitudinal Change in CSF Biomarkers in Autosomal-Dominant Alzheimer’s Disease
- Anne M. Fagan, et. al.
- ↵*Corresponding author. E-mail: fagana@neuro.wustl.edu
Abstract
Clinicopathological evidence suggests that the pathology of Alzheimer’s disease (AD) begins many years before the appearance of cognitive symptoms. Biomarkers are required to identify affected individuals during this asymptomatic (“preclinical”) stage to permit intervention with potential disease-modifying therapies designed to preserve normal brain function. Studies of families with autosomal-dominant AD (ADAD) mutations provide a unique and powerful means to investigate AD biomarker changes during the asymptomatic period. In this biomarker study, we collected cerebrospinal fluid (CSF), plasma, and in vivo amyloid imaging cross-sectional data at baseline in individuals from ADAD families enrolled in the Dominantly Inherited Alzheimer Network. Our study revealed reduced concentrations of CSF amyloid-β1–42 (Aβ1–42) associated with the presence of Aβ plaques, and elevated concentrations of CSF tau, ptau181 (phosphorylated tau181), and VILIP-1 (visinin-like protein-1), markers of neurofibrillary tangles and neuronal injury/death, in asymptomatic mutation carriers 10 to 20 years before their estimated age at symptom onset (EAO) and before the detection of cognitive deficits. When compared longitudinally, however, the concentrations of CSF biomarkers of neuronal injury/death within individuals decreased after their EAO, suggesting a slowing of acute neurodegenerative processes with symptomatic disease progression. These results emphasize the importance of longitudinal, within-person assessment when modeling biomarker trajectories across the course of the disease. If corroborated, this pattern may influence the definition of a positive neurodegenerative biomarker outcome in clinical trials.
- Copyright © 2014, American Association for the Advancement of Science