Sleep Replay Includes Emotions
During sleep, the hippocampus of rats replays the same pattern of neural activity that was seen during maze running earlier in the day; it is generally accepted that this replay aids memory consolidation. Wondering whether this replay can represent information other than the turns of the maze, neuroscientists at New York University gave rats a puff of air at one point along the way. This was clearly disturbing to the rats; they slowed down as they approached the area, then ran fast after passing it. During sleep, the usual hippocampal replay occurred, but at the point in replay corresponding to the place where they had been frightened, the amygdala became active as well. This expands our understanding of memory replay, as well as possibly explaining why people have nightmares following a traumatic experience.
Nature Neuroscience, Vol 20, 1634-1642.

Memory Replay Confirmed in Humans
Detecting memory replay involves implanting electrodes in rats' brains and it has not been attempted in humans, but an innovative study may have found a way to tap into the process. A group of subjects learned the features of 15 fictitious satellites, then underwent fMRI scans while viewing pictures of the satellite and again during rest, to establish the correlation of hippocampal replay activity with the individual satellites. Researchers noted that more time was spent on replay of information that had been less well remembered during testing. After a night asleep or a day awake, the participants underwent another scan, followed by another memory test. More hippocampal replay of a particular satellite during the resting scan predicted better subsequent memory for that satellite; rest replay also predicted improvement from the first to the second session, but only in the group with intervening sleep. According to the authors, this is the first evidence that hippocampal replay of individual memories occurs during rest in humans, and that this replay prioritizes weaker memories, predicts subsequent memory performance, and relates to memory improvement following sleep. bioRxiv, DOI:

Tourette's Syndrome May Enhance Learning
Tourette's syndrome is a disorder characterized by motor tics, such as head jerking and grimaces, and uncontrollable vocal outbursts, such as swearing or insulting passersby). In a study at the Hungarian Academy of Sciences in Budapest, children played a computer game that required them to quickly press a button to indicate the location of a dog as it moved about on the screen. The dog appeared to move at random, but it followed a subtle, repeated sequence. The task is an example of procedural learning—learning how to do something—as opposed to declarative learning, which involves learning information. Surprisingly, children with Tourette's became faster and more accurate than the other children without being aware of why; this is believed to be the first time this type of memory has been enhanced by a neurological condition. Assuming this result can be replicated, it is unclear how to account for it. However, it is worth noting that Tourette's involves excesssive dopamine activity in the basal ganglia; procedural learning involves the basal ganglia, and dopamine is a critical transmitter in learning at the neural level. Cortex, Vol 100, 84-94.

Gene Identified That Protects Against Brain Disease
Buildup of harmful proteins in the brain can lead to neurological diseases, such as Parkinson's and Alzheimer's. Now University of California - San Diego scientists have identified a gene that helps prevent the protein buildup. Ordinarily, errors in transfer RNA are corrected before proteins are synthesized, but if this proofreading fails it can result in production of the amino acid serine, which is then incorporated into proteins and causes protein aggregation. The gene ANKRD16 directs production of the ANKRD16 protein, which captures serine and reduces protein accumulation. Deleting the ANKRD16 gene in mice genetically predisposed to the transcription error results in increased protein buildup and neuronal death, while increasing the level of the ANKRD16 protein protects against cell death. Nature, Vol 557, 510-515.

NIH Triples Funding for Alzheimer's Research
Under pressure from a slew of failed studies and a controversial national goal to find a treatment by 2025, Congress has tripled the National Institutes of Health's budget for Alzheimer's and related dementias to $1.9 billion. Two draft spending bills for 2019, if they pass, will bring the total to $2.3 billion, which is more than 5% of NIH's overall budget. This still does not compare favorably with funding for cancer, heart disease, and AIDS; AIDS research, for example, gets $3 billion (after years of receiving 10% of the NIH budget), even though it affects far fewer people. Still, the increase is attracting researchers from other areas, who are bringing fresh ideas—much needed when the field's most widely accepted causal hypothesis has repeatedly failed to produce a truly effective treatment. Science, Aug 30, 2018.

Toward A New Drug for Alzheimer's
Results of a Phase 3 (clinical effectiveness) trial of aducanumab (see p 365 of your text) aren't expected until 2020; in the meantime, BAN2401 is showing highly promising results in both removing plaques and slowing cognitive decline. In patients receiving the highest dose, amyloid levels dropped below the dementia threshold and cognitive ability declined 30% slower than in the placebo group. The results were presented at the 2018 Alzheimer's Association International Conference. New York Times, July 25, 2018.

Preserving Synapses May Aid Alzheimer's Patients
Years before the symptoms of Alzheimer's Disease appear, the brain is already losing synapses; if we could identify people at risk and prevent this loss presumably we could reduce or eliminate the effects of the disease. German researcher Rahul Kaushik reported at the Federation of European Neuroscience Societies meeting that mice engineered to have Alzheimer's-like symptoms and treated with a synapse-bonding molecule his team designed (CPTX) had 30% more synapses than similar but untreated animals. CPTX's effect diminished over time, so the team is developing a gene therapy in the hope that the cells will produce their own synapse-binding molecule. Reported in New Scientist, Aug 8, 2018.

Clearing Senescent Glial Cells Halts Tau Aggregation
Using mice, researchers at Mayo Clinic have discovered that accumulation of senescent cells—cells which have stopped functioning but are still living—leads to buildup of the tau protein that forms neurofibrillary tangles and cognitive decline. Mice transgenically engineered to produce tau tangles had twice as many senescent astrocytes and microglia in the cortex, and a dozen times as many in the hippocampus. Treating tau-prone mice with a drug that causes cells to die when they become senescent halted tau aggregation and the loss of memory and cognitive ability. Nature, DOI: 10.1038/s41586-018-0543-y.

Some Alzheimer's May Be Triggered by Herpes Virus
Investigators have suspected a link between viruses and Alzheimer's, but studies have not provided definitive evidence. Researchers studying 622 brains from Alzheimer's patients and 322 from unaffected donors discovered that many of the genes affected in Alzheimer's are involved in the body's defense against viruses. Looking closer, they found evidence of significantly greater exposure to human herpes viruses 6A (HHV-6A) and 7 (HHV-7) in the patients' brains. There was evidence that these viruses activated or suppressed Alzheimer's genes, with HHV-6A alone inducing activation of seven of them. Neuron, Vol 99, 64-82. Ealier in the year a Taiwanese team reported on a group of 8362 individuals diasgnosed with herpes simplex virus infection during the year 2000. They were 2.56 times more likely to have developed dementia in the interim than were control subjects, but the risk was reduced in those who received anti-herpes medications. Neurotherapeutics, Vol 15, 417-429.