Cue-utilization in the imagination inflation effect paradigm in older adults with mild cognitive impairment.

Objective: We investigated the imagination inflation effect in healthy older adults and older adults with mild cognitive impairment (MCI) to determine whether an intervention can reduce susceptibility to these distortions, with implications for daily functioning.

Method: Fifty-seven older adults aged 69-90 participated. In Session 1, participants either: listened to an action statement being read, performed the action, or imagined performing the action.

Evidence for Improved Cognitive Health with Diet: A Narrative Review.

Background: Despite growing interest in nutrition as a behavioral intervention to improve cognitive health in clinical populations, many providers find it challenging to provide specific nutritional recommendations. We aimed to review and synthesize current empirical research on this topic and provide considerations for healthcare providers working with adults who wish to optimize their cognition via dietary improvements.

Methods: We performed a narrative review of research published between January 2009 and May 2021 on 5 popular dietary interventions: the Mediterranean diet, Dietary Approaches to Stop Hypertension (DASH), the Mediterranean-DASH Intervention Diet for Neurodegenerative Delay (MIND), the ketogenic diet and intermittent fasting.

The Rey 15-Item Memory Test in US veterans.

Introduction: The Rey 15-item Test is a public-domain, memory-based performance validity test, frequently used in clinical settings. Various efforts have been made to modify the test to make it more sensitive and more robust to effects of lower education and intelligence. The most promising of these is the addition of a recognition trial to the existing free recall paradigm.

Cognitive Impairment and Predicting Response to Treatment in an Intensive Clinical Program for Post-9/11 Veterans With Posttraumatic Stress Disorder.

Objective: This study examined whether objectively measured pretreatment cognitive impairment predicted worse response to treatment for posttraumatic stress disorder. Participants were 113 veterans and active duty service members who participated in a new multidisciplinary 2-week intensive clinical program that included individual trauma-focused cognitive-behavioral therapy, group psychotherapy, psychoeducation, skills-building groups, and complementary and alternative medicine treatments (mean age: 39.7 years [SD=8.

The Aging Well through Interaction and Scientific Education (AgeWISE) Program.

Objective: We conducted a randomized controlled trial of the Aging Well through Interaction and Scientific Education (AgeWISE) program, a 12-week manualized cognitive rehabilitation program designed to provide psychoeducation to older adults about the aging brain, lifestyle factors associated with successful brain aging, and strategies to compensate for age related cognitive decline.

Methods: Forty-nine cognitively intact participants ≥ 60 years old were randomly assigned to the AgeWISE program (n = 25) or a no-treatment control group (n = 24). Questionnaire data were collected prior to group assignment and post intervention.

Performance validity and processing speed in a VA Polytrauma sample.

Objective: While recognition memory has been the primary tool for the assessment of performance validity in neuropsychological evaluations, some consideration has also been given to embedded measures from other cognitive domains, including processing speed. The present study evaluated the classification accuracy of several speed-based measures in a Veterans Affairs Medical Center Polytrauma sample.

Method: The present sample consisted of 114 military veterans (Mean age = 35.

Copy number variants are a common cause of non-syndromic hearing loss.

Background: Copy number variants (CNVs) are a well-recognized cause of genetic disease; however, methods for their identification are often gene-specific, excluded as 'routine' in screens of genetically heterogeneous disorders, and not implemented in most next-generation sequencing pipelines. For this reason, the contribution of CNVs to non-syndromic hearing loss (NSHL) is most likely under-recognized. We aimed to incorporate a method for CNV identification as part of our standard analysis pipeline and to determine the contribution of CNVs to genetic hearing loss.

Orexin gene therapy restores the timing and maintenance of wakefulness in narcoleptic mice.

Study Objectives: Narcolepsy is caused by selective loss of the orexin/hypocretin-producing neurons of the hypothalamus. For patients with narcolepsy, chronic sleepiness is often the most disabling symptom, but current therapies rarely normalize alertness and do not address the underlying orexin deficiency. We hypothesized that the sleepiness of narcolepsy would substantially improve if orexin signaling were restored in specific brain regions at appropriate times of day.

Dorsal/ventral parcellation of the amygdala: relevance to impulsivity and aggression.

Investigations into the specific association of amygdala volume, a critical aspect of the fronto-limbic emotional circuitry, and aggression have produced results broadly consistent with the 'larger is more powerful' doctrine. However, recent reports suggest that the ventral and dorsal aspects of the amygdala play functionally specific roles, respectively, in the activation and control of behavior. Therefore, parceling amygdala volume into dorsal and ventral components might prove productive in testing hypotheses regarding volumetric association to aggression, and impulsivity, a related aspect of self-control.

Orexin receptor 2 expression in the posterior hypothalamus rescues sleepiness in narcoleptic mice.

Narcolepsy is caused by a loss of orexin/hypocretin signaling, resulting in chronic sleepiness, fragmented non-rapid eye movement sleep, and cataplexy. To identify the neuronal circuits underlying narcolepsy, we produced a mouse model in which a loxP-flanked gene cassette disrupts production of the orexin receptor type 2 (OX2R; also known as HCRTR2), but normal OX2R expression can be restored by Cre recombinase. Mice lacking OX2R signaling had poor maintenance of wakefulness indicative of sleepiness and fragmented sleep and lacked any electrophysiological response to orexin-A in the wake-promoting neurons of the tuberomammillary nucleus.

Effects of daily snack food intake on food reinforcement depend on body mass index and energy density.

Background: The reinforcing value of food plays a role in food consumption. We have shown previously that daily intake of a high-energy-density (HED) snack food decreases food reinforcement and food liking in nonobese women but increases food reinforcement and decreases food liking in obese women.

Objective: These previous studies were conducted with the use of only HED snack foods.

Loss of hypocretin (orexin) neurons with traumatic brain injury.

Chronic, daytime sleepiness is a major, disabling symptom for many patients with traumatic brain injury (TBI), but thus far, its etiology is not well understood. Extensive loss of the hypothalamic neurons that produce the wake-promoting neuropeptide hypocretin (orexin) causes the severe sleepiness of narcolepsy, and partial loss of these cells may contribute to the sleepiness of Parkinson disease and other disorders. We have found that the number of hypocretin neurons is significantly reduced in patients with severe TBI.

Orexin neurons are necessary for the circadian control of REM sleep.

Study Objectives: The orexin-producing neurons are hypothesized to be essential for the circadian control of sleep/wake behavior, but it remains unknown whether these rhythms are mediated by the orexin peptides or by other signaling molecules released by these neurons such as glutamate or dynorphin. To determine the roles of these neurotransmitters, we examined the circadian rhythms of sleep/wake behavior in mice lacking the orexin neurons (ataxin-3 [Atx] mice) and mice lacking just the orexin neuropeptides (orexin knockout [KO] mice).

Design: We instrumented mice for recordings of sleep-wake behavior, locomotor activity (LMA), and body temperature (Tb) and recorded behavior after 6 days in constant darkness.

Do enteric neurons make hypocretin?

Hypocretins (orexins) are wake-promoting neuropeptides produced by hypothalamic neurons. These hypocretin-producing cells are lost in people with narcolepsy, possibly due to an autoimmune attack. Prior studies described hypocretin neurons in the enteric nervous system, and these cells could be an additional target of an autoimmune process.