Nutritional Status and Risks of Cognitive Decline and Incident Neurocognitive Disorders: Singapore Longitudinal Ageing Studies.

BACKGROUND: Studies suggest that nutritional interventions using the whole diet approach such as the Mediterranean diet may delay cognitive decline and dementia onset. However, substantial numbers of older adults are non-adherent to any ideally healthy dietary pattern and are at risk of malnutrition. OBJECTIVE: The present study investigated the relationship between global malnutrition risk and onsets of cognitive decline and neurocognitive disorders (NCD), including mild cognitive impairment (MCI) or dementia in community-dwelling older adults. METHODS: Participants aged ≥ 55 years in the Singapore Longitudinal Ageing Studies (SLAS) were assessed at baseline using the Elderly Nutritional Indicators for Geriatric Malnutrition Assessment (ENIGMA) and followed up 3-5 years subsequently on cognitive decline (MMSE drop ≥ 2) among 3128 dementia-free individuals, and incident neurocognitive disorders (NCD) among 2640 cognitive normal individuals. RESULTS: Individuals at high nutritional risk score (≥ 3) were more likely to develop cognitive decline (OR=1.42, 95%CI=1.01-1.99) and incident MCI-or-dementia (OR=1.64, 95%CI=1.03-2.59), controlling for age, sex, ethnicity, low education, APOE-e4, hearing loss, physical, social, and mental activities, depressive symptoms, smoking, alcohol, central obesity, hypertension, diabetes, low HDL, high triglyceride, cardiac disease, and stroke. Among ENIGMA component indicators, low albumin at baseline was associated with cognitive decline and incident NCD, and 5 or more drugs used, few fruits/vegetables/milk products daily, and low total cholesterol were associated with incident NCD. CONCLUSION: The ENIGMA measure of global malnutrition risk predicts cognitive decline and incident neurocognitive disorders, suggesting the feasibility of identifying vulnerable subpopulations of older adults for correction of malnutrition risk to prevent neurocognitive disorders.

The Independent Role of Inflammation in Physical Frailty among Older Adults with Mild Cognitive Impairment and Mild-to-Moderate Alzheimer's Disease.

OBJECTIVES: To examine the independent and combined effects of inflammation and endocrine dysregulation on (i) baseline frailty status and (ii) frailty progression at one year, among cognitively impaired community dwelling older adults. DESIGN: Prospective cohort study. SETTING: Tertiary Memory Clinic. METHODS: We recruited patients with mild cognitive impairment and mild-moderate Alzheimer's disease. Physical frailty status was assessed at baseline and 1-year. Blood biomarkers of systemic inflammation [interleukin-6 (IL-6), tumour necrosis factor-α (TNF-α)] and anabolic hormones [insulin-like growth factor-1 (IGF-1), dehydroepiandrosterone sulphate (DHEAS)] were measured at baseline and examined in relation to physical frailty status at baseline and progression at 1-year. Each subject was categorized as (i) neither pro-inflammatory nor endocrine deficient, (ii) pro-inflammatory (IL-6 or TNF-α, or both, being in highest quartile) but not endocrine deficient, (iii) endocrine deficient (IGF-1 or DHEAS, or both, being in lowest quartile) but not pro-inflammatory and (iv) both pro-inflammatory and endocrine deficient. RESULTS: Twenty (20.2%) of 99 subjects were physically frail at baseline. There was no association between severity of cognitive impairment and baseline frailty status, but the frail group had significantly greater hippocampal atrophy (median MTA: 2 (2-3) vs 1 (1-2), p=0.010). TNF-α was significantly higher in subjects who were physically frail at baseline (median TNF-α: 1.30 (0.60-1.40) vs 0.60 (0.50-1.30) pg/mL, p=0.035). In multiple logistic regression adjusted for age and gender, a pro-inflammatory state in the absence of concomitant endocrine deficiency was significantly associated with physical frailty at baseline (OR=4.99, 95% C.I 1.25-19.88, p=0.023); this was no longer significant when MTA score was included in the model. Isolated pro-inflammatory state (without endocrine deficiency) significantly increased the odds of frailty progression (OR=4.06, 95% CI 1.09-15.10, p=0.037) at 1-year. The combination pro-inflammatory and endocrine deficient state was not significantly associated with either baseline or progressive physical frailty. CONCLUSION: A pro-inflammatory state exerts differential effects on physical frailty, contributing to the increased risk of baseline and progressive frailty only in the absence of a concomitant endocrine deficient state, with potential mediation via neurodegeneration.

Cannabis use in patients with multiple sclerosis.

INTRODUCTION: Little is known about the extent and patterns of cannabis use in people with multiple sclerosis (MS). METHODS: MS patients attending neurology outpatient clinics at two hospitals in London and one in Kent, UK completed a questionnaire. RESULTS: Questionnaires were completed by 254/337 (75%) MS patients. Forty-three per cent had used cannabis at some stage (ever users). Of these, 68% (75/110) had used cannabis to alleviate symptoms of MS (MS-related cannabis use). Forty-six (18%) had used cannabis in the last month (current users), of whom 12% (31/254) had used it for symptom relief. Being married or having a long-term partner, tobacco smokers and increasing disability were independent risk factors for MS-related cannabis use. Compared to patients who could walk unaided, cannabis use was more likely in those who were chair-bound (adjusted OR 2.47; 1.10-5.56) or only able to walk with an aid (adjusted OR 1.56; 0.90-3.60). Pain and spasms were common reasons for cannabis use. Seventy-one per cent of individuals who had never used cannabis said they would try the drug if it were available on prescription. CONCLUSION: A large proportion of MS patients had tried cannabis for symptom control, however current use was small. A subgroup with greater disability appears to derive some symptomatic benefit.

Bedside clinical methods useful as screening test for aspiration in elderly patients with recent and previous strokes.

INTRODUCTION: This study was undertaken to ascertain the usefulness of clinical screening tools for dysphagia in a heterogeneous group of older stroke patients. The usefulness of bedside clinical assessment tools for detecting dysphagia on different consistencies of feeds was also studied. MATERIALS AND METHODS: Fifty patients referred to a speech therapist for the assessment of possible dysphagia were recruited. The clinical tools studied included the water swallow test, the oxygen desaturation test and the combination of both tests (termed "clinical aspiration test"). The outcomes of the clinical assessments were compared with a fibreoptic endoscopic examination of swallowing (FEES) conducted at the same sitting. Fifty patients underwent an examination of their ability to swallow 50 mL of water in 10-mL aliquots. They underwent a FEES with different food consistencies by a speech therapist and oxygen saturation with pulse oximetry was monitored during the procedure. Oxygen desaturation of more than 2% was considered to be clinically significant. RESULTS: The water swallow test had a sensitivity of 79.4% and specificity of 62.5% for the detection of aspiration, with a positive predictive value (PPV) of 81.8% and a negative predictive value (NPV) of 58.8%. The oxygen desaturation test had a sensitivity of 55.9% and a specificity of 100% with PPV of 100% and NPV of 51.6%. When both tests were combined, a sensitivity of 94.1% and a specificity of 62.5% was attained, with PPV of 84.2% and NPV of 83.3%. Using the clinical assessment test, we were able to pick up 3 aspirators who would otherwise have been missed if they were assessed with the water swallow test using thin fluids alone. CONCLUSION: Simple clinical assessment tools can be used to screen for dysphagia in a heterogeneous group of older patients with stroke disease, and clinical testing using feeds of different consistencies should be considered.

Axotomy increases glycogen phosphorylase activity in motoneurones.

The relative distribution of glycogen phosphorylase a and b in the lumbar spinal cord of the adult rat following either transection or crush of the sciatic nerve has been studied. The activity of the glycogen phosphorylase was measured histochemically by its capacity to convert glucose-1-phosphate to glycogen which was then stained with iodine. Prior to any treatment, the enzyme was largely in its inactive b form. Sciatic section and crush produced a transient (24 h) decrease in the amount of the active glycogen phosphorylase a in the sciatic motoneurone pool. Fourteen days post-transection, but not crush, a marked increase in the level of the active glycogen phosphorylase a form of the enzyme could be detected in the axotomised motoneurones which persisted for up to 6 weeks. No equivalent changes occurred in the axotomized dorsal root ganglion cells. Glycogen phosphorylase although normally present in neurones in its inactive b form can be converted to the active a form by calcium or adenosine 3':5'-phosphate. The substantial increase in the level of glycogen phosphorylase a in axotomized motoneurones may be a reflection of an increased calcium influx into these cells due to the development of abnormally hyperexcitable membranes and the appearance of dendritic spikes that is known to occur in these motoneurones.