Computerised working memory‐based cognitive remediation therapy does not affect Reading the Mind in The Eyes test performance or neural activity during a Facial Emotion Recognition test in psychosis

Working memory‐based cognitive remediation therapy (CT) for psychosis has recently been associated with broad improvements in performance on untrained tasks measuring working memory, episodic memory and IQ, and changes in associated brain regions. However, it is unclear whether these improvements transfer to the domain of social cognition and neural activity related to performance on social cognitive tasks. We examined performance on the Reading the Mind in the Eyes test (Eyes test) in a large sample of participants with psychosis who underwent working memory‐based CT (N = 43) compared to a control group of participants with psychosis (N = 35). In a subset of this sample, we used functional magnetic resonance imaging (fMRI) to examine changes in neural activity during a facial emotion recognition task in participants who underwent CT (N = 15) compared to a control group (N = 15). No significant effects of CT were observed on Eyes test performance or on neural activity during facial emotion recognition, either at p < 0.05 family‐wise error or at a p < 0.001 uncorrected threshold, within a priori social cognitive regions of interest. This study suggests that working memory‐based CT does not significantly impact an aspect of social cognition which was measured behaviourally and neurally. It provides further evidence that deficits in the ability to decode mental state from facial expressions are dissociable from working memory deficits, and suggests that future CT programmes should target social cognition in addition to working memory for the purposes of further enhancing social function.     

Normalized activation in the somatosensory cortex 30 years following nerve repair in children: an fMRI study

The clinical outcome following a peripheral nerve injury in the upper extremity is generally better in young children than in teenagers and in adults, but the mechanism behind this difference is unknown. In 28 patients with a complete median nerve injury sustained at the ages of 1–13 years (n = 13) and 14–20 years (n = 15), the cortical activation during tactile finger stimulation of the injured and healthy hands was monitored at a median time since injury of 28 years using functional magnetic resonance imaging (fMRI) at 3 Tesla. The results from the fMRI were compared with the clinical outcome and electroneurography. The cortical activation pattern following sensory stimulation of the median nerve‐innervated fingers was dependent on the patient's age at injury. Those injured at a young age (1–13 years) had an activation pattern similar to that of healthy controls. Furthermore, they showed a clinical outcome significantly superior (P = 0.001) to the outcome in subjects injured at a later age; however, electroneurographical parameters did not differ between the groups. In subjects injured at age 14–20 years, a more extended activation of the contralateral hemisphere was seen in general. Interestingly, these patients also displayed changes in the ipsilateral hemisphere where a reduced inhibition of somatosensory areas was seen. This loss of ipsilateral inhibition correlated to increasing age at injury as well as to poor recovery of sensory functions in the hand. In conclusion, cerebral changes in both brain hemispheres may explain differences in clinical outcome following a median nerve injury in childhood or adolescence.     

EUROPEAN HERBS WITH CHOLINERGIC ACTIVITIES: POTENTIAL IN DEMENTIA THERAPY

We investigated plants reputed in herbal encyclopedias to enhance memory or alleviate mental disorder for cholinergic activities since this transmitter system has been implicated in memory and dementia. Crude extracts were applied to human brain homogenates to determine whether any inhibit acetylcholinesterase. Of three plants with reputed memory enhancing properties (rosemary, sage and balm), extracts of sage (Salvia officinalis) inhibited the brain enzyme in a concentration dependant manner. 50% enzyme inhibition was obtained at a concentration of 0.07 μg essential oil per ml and 1.5 mg fresh herb per ml. None of the known and commercially available chemical constituents of sage oil so far tested (borneol, caffeic acid, camphor, cineol or thujone) inhibited the enzyme, indicating that the active plant constituent(s) may be an as yet unidentified compound(s). In parallel studies, plants with insecticide or vermifuge (antihelminthic) properties, which frequently depend on cholinergic activities, were examined for cholinergic receptor interactions. Crude alcoholic extracts of wormwood, balm and angelica displaced nicotine binding to the nicotinic receptor in a concentration dependant manner, with IC₅₀ values ranging from 3–15 mg/ml. Components of these plants may be relevant in relation to dementia therapy since there is a loss of nicotinic receptors in Alzheimer's disease and related disorders and stimulation of the nicotinic receptor leads to increased receptor numbers.     

The Rise of a New Psychoactive Agent: Salvia divinorum

Since the 1990s, there has been a rise in the availability and recreational use of a herbal plant called Salvia divinorum. Numerous internet websites have advertised it for sale as a legal herbal alternative to illegal hallucinogens. Initial data surveying use has indicated many young adults are obtaining and using this herb for its psychoactive properties. Reported methods of ingestion for the plant include chewing, and smoking leaves or fortified extracts. Subjective effects of the plant include, affect changes, psychedelic-like changes in perception, and even loss of consciousness. Although the pharmacological properties and possible antidepressant effects have been studied in recent years, little information is known about potential negative impact resulting from recreational use, and scant information about Salvia divinorum currently exists in the psychological and substance abuse literature. While Salvia divinorum appears to be a substance with some therapeutic potential, it also poses some significant dangers as a substance of varying legal status with a potential for abuse.     

Inhibitory effects of heterotopic noxious counter‐stimulation on perception and brain activity related to Aβ‐fibre activation

Heterotopic noxious counter‐stimulation (HNCS) inhibits pain and pain processes through cerebral and cerebrospinal mechanisms. However, it is unclear whether HNCS inhibits non‐nociceptive processes, which needs to be clarified for a better understanding of HNCS analgesia. The aim of this study was to examine the effects of HNCS on perception and scalp somatosensory evoked potentials (SEPs). Seventeen healthy volunteers participated in two counter‐balanced sessions, including non‐nociceptive (selective Aβ‐fibre activation) or nociceptive electrical stimulation, combined with HNCS. HNCS was produced by a 20‐min cold pressor test (left hand) adjusted individually to produce moderate pain (mean ± SEM: 42.5 ± 5.3 on a 0–100 scale, where 0 is no pain and 100 the worst pain imaginable). Non‐nociceptive electrical stimulation was adjusted individually at 80% of pain threshold and produced a tactile sensation in every subject. Nociceptive electrical stimulation was adjusted individually at 120% of RIII‐reflex threshold and produced moderate pain (45.3 ± 4.5). Shock sensation was significantly decreased by HNCS compared with baseline for non‐nociceptive (P < 0.001) and nociceptive (P < 0.001) stimulation. SEP peak‐to‐peak amplitude at Cz was significantly decreased by HNCS for non‐nociceptive (P < 0.01) and nociceptive (P < 0.05) stimulation. These results indicate that perception and brain activity related to Aβ‐fibre activation are inhibited by HNCS. The mechanisms of this effect remain to be investigated to clarify whether it involves inhibition of spinal wide‐dynamic‐range neurons by diffuse noxious inhibitory controls, supraspinal processes or both.     

Non‐invasive brain stimulation for fine motor improvement after stroke: a meta‐analysis

The aim of this study was to determine whether non‐invasive brain stimulation (NIBS) techniques improve fine motor performance in stroke. We searched PubMed, EMBASE, Web of Science, SciELO and OpenGrey for randomized clinical trials on NIBS for fine motor performance in stroke patients and healthy participants. We computed Hedges’ g for active and sham groups, pooled data as random‐effects models and performed sensitivity analysis on chronicity, montage, frequency of stimulation and risk of bias. Twenty‐nine studies (351 patients and 152 healthy subjects) were reviewed. Effect sizes in stroke populations for transcranial direct current stimulation and repeated transcranial magnetic stimulation were 0.31 [95% confidence interval (CI), 0.08–0.55; P = 0.010; Tau², 0.09; I², 34%; Q, 18.23; P = 0.110] and 0.46 (95% CI, 0.00–0.92; P = 0.05; Tau², 0.38; I², 67%; Q, 30.45; P = 0.007). The effect size of non‐dominant healthy hemisphere transcranial direct current stimulation on non‐dominant hand function was 1.25 (95% CI, 0.09–2.41; P = 0.04; Tau², 1.26; I², 93%; Q, 40.27; P < 0.001). Our results show that NIBS is associated with gains in fine motor performance in chronic stroke patients and healthy subjects. This supports the effects of NIBS on motor learning and encourages investigation to optimize their effects in clinical and research settings.     

Salvia divinorum: An overview of the usage,misuse, and addiction processes

Salvia divinorum, a sage plant with leaves that can produce a psychoactive high, has been used for hundreds of years for its psycho‐mimetic effects in religious rituals in South America. Salvia has now become popular mainly with adolescents and young adults for the short‐lived relatively pleasant experiences many consider a “legal high” and its ready availability through Internet purchases. The main (psycho)active compound in salvia is Salvinorin A, a potent κ‐opioid agonist and although the short and long‐term effects have not been examined in sufficient detail, it is widely believed to have low addictive potential and low toxicity. Recent findings, however, seem to suggest that Salvinorin A can precipitate psychiatric symptoms and negatively affect cognition. Its ready availability and increasingly widespread use requires clinicians to have knowledge and awareness of its effects.     

Cognitive and psychiatric symptoms in genetically determined Parkinson’s disease: a systematic review

The aim was to review the existing reports on cognitive and behavioural symptoms in monogenic forms of Parkinson’s disease (PD) and to identify recurring patterns of clinical manifestations in those with specific mutations. A systematic literature search was conducted to retrieve observational studies of monogenic PD. Data pertaining to cognitive and psychiatric manifestations were extracted using standardized templates. The PRISMA guidelines were followed. Of the 1889 citations retrieved, 95 studies on PD‐related gene mutations were included: 35 in SNCA, 35 in LRRK2, four in VPS35, 10 in Parkin, three in DJ1 and eight in PINK1. Nineteen studies (20%) provided adequate data from comprehensive cognitive assessment and 31 studies (32.6%) outlined psychiatric manifestations through the use of neuropsychiatric scales. Cognitive impairment was reported in all monogenic PD forms with variable rates (58.8% PINK1, 53.9% SNCA, 50% DJ1, 29.2% VPS35, 15.7% LRRK2 and 7.4% Parkin). In this regard, executive functions and attention were the domains most affected. With respect to psychiatric symptoms, depression was the most frequent symptom, occurring in 37.5% of PINK1 cases and 41.7% of VPS35 and LRRK2 cases. Co‐occurrence of cognitive decline with visual hallucinations was evidenced. Widespread accumulation of Lewy bodies, distinctive of SNCA, PINK1 and DJ1 mutations, results in higher rates of cognitive impairment. Similarly, a higher degree of visual hallucinations is observed in SNCA mutations, probably owing to the more widespread accumulation. The lower rates of α‐synuclein pathology in LRRK2 and Parkin may underpin the more benign disease course in these patients.     

Brain‐Derived Neurotrophic Factor and Substrate Utilization Following Acute Aerobic Exercise in Obese Individuals

Brain‐derived neurotrophic factor (BDNF) serves as a vital regulator of neuronal proliferation and survival, and has been shown to regulate energy homeostasis, glucose metabolism and body weight maintenance. Elevated concentrations of plasma BDNF have been associated with obesity and type 2 diabetes mellitus. Acute aerobic exercise transiently increases circulating BDNF, potentially correcting obesity‐related metabolic impairment. The present study aimed to compare acute aerobic exercise elicited BDNF responses in obese and normal‐weight subjects. Furthermore, we aimed to investigate whether acute exercise‐induced plasma BDNF elevations would be associated with improved indices of insulin resistance, as well as substrate utilization [carbohydrate oxidation (CHOoxi) and fat oxidation (FAToxi)]. Twenty‐two healthy, untrained subjects [11 obese (four men and seven women; age = 22.91 ± 4.44 years; body mass index = 35.72 ± 4.17 kg/m²) and 11 normal‐weight (five men and six women; age = 23.27 ± 2.24 years; body mass index = 21.89 ± 1.63 kg/m²)] performed 30 min of continuous submaximal aerobic exercise at 75% maximal oxygen consumption. Our analyses showed that the BDNF response to acute aerobic exercise was similar in obese and normal‐weight subjects across time (time: P = 0.015; group: P = not significant) and was not associated with indices of IR. Although no differences in the rates of CHOoxi and FAToxi were found between both groups, total relative energy expenditure was significantly lower in obese subjects compared to normal‐weight subjects (3.53 ± 0.25 versus 5.59 ± 0.85; P < 0.001). These findings suggest that acute exercise‐elicited BDNF elevation may not be sufficient to modulate indices of IR or the utilization of either carbohydrates or fats in obese individuals.     

Changes in orexinergic immunoreactivity of the piglet hypothalamus and pons after exposure to chronic postnatal nicotine and intermittent hypercapnic hypoxia

We recently showed that orexin expression in sudden infant death syndrome (SIDS) infants was reduced by 21% in the hypothalamus and by 40–50% in the pons as compared with controls. Orexin maintains wakefulness/sleeping states, arousal, and rapid eye movement sleep, abnormalities of which have been reported in SIDS. This study examined the effects of two prominent risk factors for SIDS, intermittent hypercapnic hypoxia (IHH) (prone‐sleeping) and chronic nicotine exposure (cigarette‐smoking), on orexin A (OxA) and orexin B (OxB) expression in piglets. Piglets were randomly assigned to five groups: saline control (n = 7), air control (n = 7), nicotine [2 mg/kg per day (14 days)] (n = 7), IHH (6 min of 7% O₂/8% CO₂ alternating with 6‐min periods of breathing air, for four cycles) (n = 7), and the combination of nicotine and IHH (N + IHH) (n = 7). OxA/OxB expression was quantified in the central tuberal hypothalamus [dorsal medial hypothalamus (DMH), perifornical area (PeF), and lateral hypothalamus], and the dorsal raphe, locus coeruleus of the pons. Nicotine and N + IHH exposures significantly increased: (i) orexin expression in the hypothalamus and pons; and (ii) the total number of neurons in the DMH and PeF. IHH decreased orexin expression in the hypothalamus and pons without changing neuronal numbers. Linear relationships existed between the percentage of orexin‐positive neurons and the area of pontine orexin immunoreactivity of control and exposure piglets. These results demonstrate that postnatal nicotine exposure increases the proportion of orexin‐positive neurons in the hypothalamus and fibre expression in the pons, and that IHH exposure does not prevent the nicotine‐induced increase. Thus, although both nicotine and IHH are risk factors for SIDS, it appears they have opposing effects on OxA and OxB expression, with the IHH exposure closely mimicking what we recently found in SIDS.     

Chronic depressive symptomatology and CSF amyloid beta and tau levels in mild cognitive impairment

Objectives

To investigate the association between chronic subsyndromal symptoms of depression (SSD), cerebrospinal fluid (CSF) biomarkers, and neuropsychological performance in individuals with mild cognitive impairment (MCI).

Methods

Participants included 238 older adults diagnosed with MCI from the Alzheimer's Disease Neuroimaging Initiative repository with cognitive and CSF amyloid beta (Aβ_1–42), total tau (t‐tau), and phosphorylated tau (p‐tau) data. The Neuropsychiatric Inventory identified individuals with chronic endorsement (SSD group N = 80) or no endorsement (non‐SSD group N = 158) of depressive symptoms across timepoints. CSF biomarker and cognitive performance were evaluated with linear regression models adjusting for age, education, gender, APOE genotype, global cognitive status, and SSD group.

Results

As compared to the non‐SSD group, the SSD group displayed lower CSF Aβ_1–42 levels (β = ?24.293, S.E. = 6.345, P < 0.001). No group differences were observed for CSF t‐tau (P = 0.497) or p‐tau levels (P = 0.392). Lower CSF Aβ_1–42 levels were associated with poorer performance on learning (β = 0.041, S.E. = 0.018, P = 0.021) and memory (β = ?0.012, S.E. = 0.005, P = 0.031) measures, whereas higher CSF t‐tau levels were associated with poorer performance on measures of global cognition (β = 0.022, S.E = 0.008, P = 0.007) and language (β = ?0.010, S.E = 0.004, P = 0.019). SSD was independently associated with diminished global cognition, learning and memory, language, and executive function performance over and above the effects of CSF biomarkers (all P < 0.05).

Conclusions

MCI participants with SSD displayed diminished CSF Aβ_1–42 levels but did not differ from non‐SSD controls in CSF tau levels. Additionally, CSF biomarkers and SSD independently accounted for variance in cognitive performance, suggesting that these factors may uniquely confer cognitive risk in MCI.     

Enhanced motivation of cognitive control in Parkinson's disease

Motor and cognitive deficits in Parkinson's disease (PD) have been argued to reflect motivational deficits. In prior work, however, we have shown that motivation of cognitive control is paradoxically potentiated rather than impaired in Parkinson's disease. This is particularly surprising given the fact that Parkinson's disease is often accompanied by depression, a prototypical disorder of motivation. To replicate our previous finding and assess the effects of depression, we investigated performance of PD patients with (n = 22) and without depression (history) (n = 23) and age‐matched healthy controls (n = 23) on a task specifically designed to measure the effect of reward motivation on task‐switching. We replicated previous findings by showing contrasting effects of reward motivation on task‐switching in PD patients and age‐matched healthy controls. While the promise of high versus low reward improved task‐switching in PD, it tended to impair task‐switching in age‐matched healthy controls. There were no effects of a depression (history) diagnosis in PD patients. These findings reinforce prior observations that Parkinson's disease is accompanied by enhanced incentive motivation of cognitive control and highlight the potential of incentive motivational strategies for overcoming cognitive deficits in Parkinson's disease.     

Can you detect early dementia from an email? A proof of principle study of daily computer use to detect cognitive and functional decline

Objective

To determine whether multiple computer use behaviours can distinguish between cognitively healthy older adults and those in the early stages of cognitive decline, and to investigate whether these behaviours are associated with cognitive and functional ability.

Methods

Older adults with cognitive impairment (n = 20) and healthy controls (n = 24) completed assessments of cognitive and functional abilities and a series of semi‐directed computer tasks. Computer use behaviours were captured passively using bespoke software.

Results

The profile of computer use behaviours was significantly different in cognitively impaired compared with cognitively healthy control participants including more frequent pauses, slower typing, and a higher proportion of mouse clicks. These behaviours were significantly associated with performance on cognitive and functional assessments, in particular, those related to memory.

Conclusion

Unobtrusively capturing computer use behaviours offers the potential for early detection of neurodegeneration in non‐clinical settings, which could enable timely interventions to ultimately improve long‐term outcomes.     

Octodon degus: A Model for the Cognitive Impairment Associated with Alzheimer's Disease

Octodon degus (O. degus) is a diurnal rodent that spontaneously develops several physiopathological conditions, analogous in many cases to those experienced by humans. In light of this, O. degus has recently been identified as a very valuable animal model for research in several medical fields, especially those concerned with neurodegenerative diseases in which risk is associated with aging. Octodon degus spontaneously develops β‐amyloid deposits analogous to those observed in some cases of Alzheimer's disease (AD). Moreover, these deposits are thought to be the key feature for AD diagnosis, and one of the suggested causes of cell loss and cognitive deficit. This review aims to bring together information to support O. degus as a valuable model for the study of AD.     

No evidence for a BRD2 promoter hypermethylation in blood leukocytes of Europeans with juvenile myoclonic epilepsy

Juvenile myoclonic epilepsy (JME) is a common syndrome of genetic generalized epilepsies (GGEs). Linkage and association studies suggest that the gene encoding the bromodomain‐containing protein 2 (BRD2) may increase risk of JME. The present methylation and association study followed up a recent report highlighting that the BRD2 promoter CpG island (CpG76) is differentially hypermethylated in lymphoblastoid cells from Caucasian patients with JME compared to patients with other GGE subtypes and unaffected relatives. In contrast, we found a uniform low average percentage of methylation (<4.5%) for 13 CpG76‐CpGs in whole blood cells from 782 unrelated European Caucasians, including 116 JME patients, 196 patients with genetic absence epilepsies, and 470 control subjects. We also failed to confirm an allelic association of the BRD2 promoter single nucleotide polymorphism (SNP) rs3918149 with JME (Armitage trend test, P = 0.98), and we did not detect a substantial impact of SNP rs3918149 on CpG76 methylation in either 116 JME patients (methylation quantitative trait loci [meQTL], P = 0.29) or 470 German control subjects (meQTL, P = 0.55). Our results do not support the previous observation that a high DNA methylation level of the BRD2 promoter CpG76 island is a prevalent epigenetic motif associated with JME in Caucasians.     

Cognition in multiple system atrophy: neuropsychological profile and interaction with mood

We evaluated cognitive functions and mood in two groups of patients with multiple system atrophy (MSA) in order to determine the influence of mood on cognitive performance. Our aim was to differentiate between parkinsonism-predominant (MSA-P) and cerebellar-predominant (MSA-C) MSA based on those parameters. Fifteen MSA-P and 10 MSA-C patients underwent neuropsychological tests that examined executive functions (working memory, response inhibition, and verbal reproduction), verbal learning and memory, verbal and visual reasoning, and processing speed. Anxiety and depression were also assessed. The findings on their cognitive performance and mood were compared to those of healthy controls and also discussed in relation to a group of Parkinson’s disease (PD) patients. The results showed that cognitive and mood characteristics could distinguish MSA-P from MSA-C and that anxiety and depression are related to cognitive decline. Compared with healthy controls, MSA-P patients showed reduced verbal retrieval (immediate, P < 0.019; long-term, P < 0.018) while MSA-C patients had difficulties in learning new verbal information (P < 0.022) and in controlling attention (P < 0.023). These data indicate that MSA-P and MSA-C appear to have, at least in part, different cognitive and mood profiles. The neuropsychological assessments of MSA patients should test for and then take into account their level of anxiety and depression, insofar as it might have an adverse effect on their cognitive performance.     

NeuroCog FX: Computerized screening of cognitive functions in patients with epilepsy

NeuroCog FX, a computerized neuropsychological screening instrument for serial examinations of patients with epilepsy and other neurological diseases, was developed to fill the gap between unspecific ratings and comprehensive assessments. Eight subtests address attention, working memory, verbal and figural memory, and language. The test duration is less than 30 min. In research contexts, the test can be applied at multiple sites by nonacademic personnel. Normative data were recorded from healthy subjects (N = 244, age range = 16–75 years; retest: N = 44; validation: N = 40) and unselected patients from an epileptology unit (N = 212; retest: N = 94; validation: N = 126). Psychometric analyses confirmed sufficient reliability and concurrent validity, particularly in patients. NeuroCog FX memory and overall performance scores showed “fair” to “good” diagnostic utility with respect to deficits revealed by established tests. NeuroCog FX provides reliable and valid measures of cognitive performance and may be used in clinical and research contexts as a screening instrument.     

Heterogeneous neuronal activity in the lateral habenula after short‐ and long‐term cocaine self‐administration in rats

Cocaine addiction is thought to be the result of drug‐induced functional changes in a neural network implicated in emotions, learning and cognitive control. Recent studies have implicated the lateral habenula (LHb) in drug‐directed behavior, especially its aversive aspects. Limited cocaine exposure has been shown to alter neuronal activity in the LHb, but the impact of long‐term drug exposure on habenula function has not been determined. Therefore, using c‐fos as a marker, we here examined neuronal activity in LHb in rats that self‐administered cocaine for either 10 or 60 days. Both the density of labeled cells and the cellular labeling intensity were measured in the lateral (LHbL) and medial (LHbM) parts of LHb. After 10 days of cocaine self‐administration, both the density and intensity of c‐fos‐positive cells were significantly increased in LHbL, but not LHbM, while after 60 days, an increased density (but not intensity) of labeled neurons in both LHbL and LHbM was observed. Most c‐fos‐labeled neurons were glutamatergic. In addition, we found increased GAD65 expression after 10 but not 60 days of cocaine self‐administration in the rostral mesencephalic tegmental nucleus. These data shed light on the complex temporal dynamics by which cocaine self‐administration alters activity in LHb circuitry, which may play an important role in the descent to compulsive drug use as a result of prolonged cocaine‐taking experience.     

A proteomics study reveals a predominant change in MaoB expression in platelets of healthy volunteers after high protein meat diet: relationship to the methylation cycle

Studies investigating the impact of high meat intake on cognition have yielded contradictory results as some show improved cognitive performance, whereas others report an increase of risk factors for dementia. However, few studies were designed to directly assess the effect of a high protein (HP) diet on both cognitive performance and corresponding biochemical parameters. A randomised intervention study was conducted with 23 healthy males (aged 19–31 years) to investigate the effects of a usual (UP) versus a HP diet on cognitive function and on the platelet proteome a well-established model for neurons. The study individuals were assigned to either a UP diet (15% energy) or a HP diet (30% energy) for 3 weeks with controlled intake of food and beverages. Blood samples were taken along with measurements of cognitive functions at the beginning and at the end of the intervention period. Among 908 reproducibly studied platelet proteins only the level of monoamine oxidase B (MaoB), a neurotransmitter degrading enzyme, decreased by 26% significantly (adjusted P value < 0.05) due to the HP diet. In addition, we found a correlation (r = 0.477; P < 0.02) between the decrease of MaoB expression and the shortened reaction time (cognitive function) which is in accordance with reports that dementia patients show increased MaoB activity. Plasma vitamin B₁₂ concentration was increased by the HP diet and correlates inversely with platelet MaoB expression (r = −0.35; P < 0.02). Healthy young males on a HP diet showed improved cognitive function and counteract well-known dementia biomarkers such as platelet MaoB and components of the methylation cycle such as vitamin B₁₂ and homocysteine.     

Cognitive functioning in severe psychiatric disorders: a general population study

In clinical samples, patients with severe psychiatric disorders are found to have cognitive impairments. Less is known whether this applies to samples derived from the general population. We aimed to study cognitive functioning in a population-based sample comprising individuals with schizophrenia, other non-affective psychoses, bipolar disorders, major depressive disorder, and controls derived from the same population. The current analysis was based on 148 persons with severe mental disorders and 66 control subjects, derived from the Psychoses in Finland study. All subjects were interviewed with SCID, and a neuropsychological test battery was administered. Subjects with schizophrenia had a generalized cognitive impairment (d = 0.43–1.07), while those with other non-affective psychoses were impaired in verbal memory and processing speed (d = 0.43–0.59). Subjects with bipolar disorders were not impaired. Unipolar major depressive disorder associated with slowed processing speed (d = 0.64). Our findings on cognitive impairments in subjects with schizophrenia and other non-affective psychoses derived from the general population support previous findings of a generalized cognitive dysfunction in these subjects. However, our results suggest that subjects with bipolar disorders from non-clinical populations may not have significant cognitive impairments. Our results emphasize the importance of using control samples derived from the same population and studied similarly as those with disorders in evaluating cognitive functioning of subjects with severe mental disorders.