Did you know? SfN’s journals, JNeurosci and eNeuro, publish high-quality papers on a broad range of neuroscience topics written by scientists around the world. In this Neuronline series, explore some of the research recently published in JNeurosci and eNeuro.
Sleep History Predicts Late-Life Alzheimer's Pathology
Sleep patterns can predict the accumulation of Alzheimer’s pathology proteins later in life, according to a new study of older men and women published in JNeurosci. These findings could lead to new sleep-based early diagnosis and prevention measures in the treatment of Alzheimer’s disease.
Alzheimer’s disease is known to be associated with disrupted sleep in addition to accumulation of tau and amyloid-β proteins in the brain, which can emerge long before characteristic memory impairments appear. Two types of hippocampal sleep waves, slow oscillations and sleep spindles, are synced in healthy individuals, but not in Alzheimer’s patients.
Matthew Walker, Joseph Winer, and colleagues at the University of California, Berkeley and colleagues found a decrease in slow oscillations/sleep spindle synchronization was associated with higher tau, while reduced slow-wave activity amplitude was associated with higher amyloid-β levels.
The researchers also found a decrease in sleep quantity of people in their 50s through 70s was associated with higher levels of amyloid-β and tau later in life. This means changes in brain activity during sleep and sleep quantity during this timeframe could serve as a warning sign for Alzheimer’s disease, allowing for early preventive care.
Read the manuscript in JNeurosci: Sleep as a Potential Biomarker of Tau and β-Amyloid Burden in the Human Brain
Researchers Identify New Hunger Pathway in the Brain
A newly identified hunger pathway in the brain can quickly modify food intake in the presence of food, according to a study of mice published in JNeurosci. This pathway could be a future target for the treatment of eating disorders.
Food intake is modified by long-term signals such as hormones and molecules released during digestion, but a newly recognized circuit in the hypothalamus can change feeding behavior on a shorter timescale.
Using fluorescent calcium imaging and electrophysiological recording, Shane Hentges and Andrew Rau at Colorado State University identified a pathway in the hypothalamus that affects food intake and body weight through release of the neurotransmitter GABA, which can occur due to the detection, rather than consumption, of food.
The researchers found that food-deprived mice exhibited more GABA-related neuron activity, indicating temporary energy states can directly affect feeding behavior. Increased knowledge of this pathway improves our understanding of how the brain controls energy balance.
Read the manuscript in JNeurosci: GABAergic Inputs to POMC Neurons Originating from the Dorsomedial Hypothalamus are Regulated by Energy State
Stem Cell Stimulation Improves Stroke Recovery
Stem cell stimulation shows promise as a potential noninvasive stroke treatment, according to research in mice published in JNeurosci. If extended to humans, this technique could greatly improve patients’ quality of life.
Ling Wei, Shang Ping Yu, and colleagues at Emory University injected neural stem cells into the brains of mice after a stroke and activated the cells through nasal administration of a protein. The stem cells activated by this new, noninvasive technique called optochemogenetics grew healthier and formed more connections compared to the stem cells that did not receive stimulation. Additionally, the mice that received both stem cells and stimulation displayed the most recovery, with some behaviors returning to pre-stroke levels.
The combination of stem cell injection and stimulation increased the likelihood of successful stroke recovery in mice. Following injection of stem cells in the damaged area of the brain with stimulation creates an ideal environment for the cells to develop and form connections with surrounding neurons.
Read the manuscript in JNeurosci: Optochemogenetics Stimulation of Transplanted iPS-NPCs Enhances Neuronal Repair and Functional Recovery after Ischemic Stroke
Retina Restructures Itself After Cell Death
Following gene therapy, the retina can restructure itself and regain normal light responses, according to research in mice published in JNeurosci. These results emphasize the plasticity of the retina and support ongoing development of treatments designed to save dying cells.
Blindness is often caused by the death of rod photoreceptors, a type of cell in the retina. Current treatments have been developed that can save dying rods, but it was not known if the retina could rebuild itself after treatment, which is a key component of regaining vision.
Jeannie Chen, Alapakkam Sampath, Greg Field, and colleagues developed a mouse model with genetically defective rods that mimic developmental blindness disorders in humans. Chen, Sampath, and Field's team examined the structure of the defective retina, as well as its responses to light, at different time points with and without gene therapy. They observed that the rods that received gene therapy not only regained normal light responses but also recovered normal connections to other retinal neurons.
Read the manuscript in JNeurosci: Activation of Rod Input in a Model of Retinal Degeneration Reverses Retinal Remodeling and Induces Formation of Functional Synapses and Recovery of Visual Signaling in the Adult Retina
