Neurological ageing factors : neurobiology of ageing and prevention of dementia

The original publication is available at http://www.cmej.org.za/index.php/cmej/indexBy the year 2000 the total human population passed the 6 billion mark. It is estimated to peak at 9 billion around 2070 before declining to 8.4 billion at the end of the century. The decline will largely be due to reduced fertility rates, improved health care and quality of life. However, currently the proportion of elderly (i.e. over 60 years of age) is 10%; this is expected to reach 34% by 2100

A new model for the pathophysiology of Alzheimer's disease: Aluminium toxicity is exacerbated by hydrogen peroxide and attenuated by an amyloid protein fragment and melatonin

Objectives. Although Alzheimer's disease (AD) is the leading cause of dementia in developed countries, there is an as yet unexplained lower prevalence of the disease in parts of Africa. AD is characterised by a catastrophic loss of neurons; free radicals (oxidative toxins) have been implicated in the destruction of the cells through the process of lipid peroxidative damage of cell membranes. Previously aluminium (Al) and a fragment of beta amyloid (Aβ 25 - 35) were shown to exacerbate tree-radical damage, while melatonin reduced this effect. The aim of the present study was: (i) to investigate the conditions detennining the toxicity of Al and Aβ 25 - 35; and (ii) to assess whether melatonin could attenuate the damage done by both aluminium and the amyloid fragment, thus suggesting a pathway for the aetiology of AD.Design. An in vitro model system was used in which free radicals were generated, causing lipid peroxidation of platelet membranes, thus simulating the disease process found in the brain.Results. 1. Al and Aβ 25 - 35 caused lipid peroxidation in the presence of the iron (II) ion (Fe2+, Al being more toxic than Aβ 25 - 35. 2. Aβ 25 - 35 attenuated the lipid peroxidation promoted by Al. 3. Hydrogen peroxide (H2O2 greatly exacerbated the toxicity of Al and Aβ 25 - 35. 4. Melatonin prevented lipid peroxidation by Al and Aβ 25 - 35 in the absence of H2O2, but only reduced the process when H2O2 was present.Conclusions. In the light of the results obtained from the present study, the following hypotheses are formulated. 1. In AD, excessive quantities of Al are taken up into the  brain, where the Al exacerbates iron-induced lipid peroxidatian in the Iysosomes. 2. In response, the normal synthetic pathway of amyloid protein is altered to produce Aβ fragments which attenuate the toxicity of Al. In the process of sequestering the Al and iron, immature plaques are formed in the brain. 3. Microglia are activated, in an attempt to destroy the plaques by secreting reactive oxygen species such as H2O2. At this point in the disease process, lipid peroxidation causes a catastrophic loss of brain cells. 4. Melatonin, together with other free radical scavengers in the brain, reduces the free-radical damage caused by Al and Aβ, except in the latter stages of the disease process. Since melatonin is produced by the pineal gland only in the dark, the excess of electric light in developed countries may help explain why AD is more prevalent in these countries than in rural Africa

Alzheimer\u27s disease and vascular dementia in developing countries: prevalence, management, and risk factors

Despite mortality due to communicable diseases, poverty, and human conflicts, dementia incidence is destined to increase in the developing world in tandem with the ageing population. Current data from developing countries suggest that age-adjusted dementia prevalence estimates in 65 year olds are high (≥5%) in certain Asian and Latin American countries, but consistently low (1–3%) in India and sub-Saharan Africa; Alzheimer\u27s disease accounts for 60% whereas vascular dementia accounts for ∼30% of the prevalence. Early-onset familial forms of dementia with single-gene defects occur in Latin America, Asia, and Africa. Illiteracy remains a risk factor for dementia. The APOE ε4 allele does not influence dementia progression in sub-Saharan Africans. Vascular factors, such as hypertension and type 2 diabetes, are likely to increase the burden of dementia. Use of traditional diets and medicinal plant extracts might aid prevention and treatment. Dementia costs in developing countries are estimated to be US$73 billion yearly, but care demands social protection, which seems scarce in these regions

The 2022 symposium on dementia and brain aging in low‐ and middle‐income countries: Highlights on research, diagnosis, care, and impact

Two of every three persons living with dementia reside in low‐ and middle‐income countries (LMICs). The projected increase in global dementia rates is expected to affect LMICs disproportionately. However, the majority of global dementia care costs occur in high‐income countries (HICs), with dementia research predominantly focusing on HICs. This imbalance necessitates LMIC‐focused research to ensure that characterization of dementia accurately reflects the involvement and specificities of diverse populations. Development of effective preventive, diagnostic, and therapeutic approaches for dementia in LMICs requires targeted, personalized, and harmonized efforts. Our article represents timely discussions at the 2022 Symposium on Dementia and Brain Aging in LMICs that identified the foremost opportunities to advance dementia research, differential diagnosis, use of neuropsychometric tools, awareness, and treatment options. We highlight key topics discussed at the meeting and provide future recommendations to foster a more equitable landscape for dementia prevention, diagnosis, care, policy, and management in LMICs. Highlights: Two‐thirds of persons with dementia live in LMICs, yet research and costs are skewed toward HICs. LMICs expect dementia prevalence to more than double, accompanied by socioeconomic disparities. The 2022 Symposium on Dementia in LMICs addressed advances in research, diagnosis, prevention, and policy. The Nairobi Declaration urges global action to enhance dementia outcomes in LMICs

Hoarding symptoms in patients on a geriatric psychiatry inpatient unit

Background. While collecting may be a nonnal behaviour, hoarding is a symptom of various psychiatric disorders, including obsessive-compulsive disorder (OCD) and obsessive-compulsive· personality disorder (OCPD). Although anecdotal reports suggest that hoarding is not uncommon in geriatric psychiatry populations, its psychopathological correlates in such samples have not been well characterised.Methods. The presence of clinically significant hoarding symptoms was screened for in 100 consecutive patients in a geriatric psychiatry inpatient unit. Both patient and collateral histories were obtained. When hoarding symptoms were present, a detailed history of their phenomenology was obtained by means of a structured questionnaire and the response of hoarding symptoms to treatment during hospitalisation was monitored.Results. Clinically significant hoarding was found in 5/100 subjects. Four of these 5 patients met DSM-IV criteria for schizophrenia (paranoid subtype), with onset of symptoms coinciding with increased symptoms of dementia The fifth patient met criteria for bipolar disorder (manic episode), also had symptoms of dementia, and had a lifelong history of hoarding. Hoarding behaviours responded to antipsychotic treatment in 3 of the 5 patients.Conclusions. A history of hoarding may be useful in many psychiatric patients, but psychopathological correlates of this symptom are likely to vary with age. In a geriatric psychiatry inpatient population hoarding was associated not with OCD or OCPD, but rather with paranoid schizophrenia and increasing symptoms of dementia Dopamine blockers appeared useful in decreasing hoarding in some patients, raising interesting questions about the neurobiology of this symptom

Zinc and platelet membrane microviscosity in Alzheimer's disease: The in vivo effect of zinc on platelet membranes and cognition

Objectives. To investigate the effects of oral zinc supplementation on: (i) plasma zinc concentrations; (ii) platelet membrane microviscosity in vivo; and (iii) cognitive function of Alzheimer's disease (AD) patients.Design. An open-labelled pilot study.Setting. University of Stellenbosch Medical School and Stikland Hospital.Subjects. Six volunteer AD patients.Outcome measures. Plasma zinc levels, platelet membrane microviscosity and cognition (MMSE and ADAS-cog tests).Results. Oral zinc supplementation (30 mg/day) did not increase plasma zinc levels significantly, but signfficantly increased platelet membrane microviscosity (P = 0.02; 6 patients). Four patients. who underwent 12 months of evaluation, showed modest cognitive improvement on psychomebic testing (Mini-Mental State Examination and the cognitive portion of the Alzheimer's Disease Assessment scale scores).Conclusions. While earlier literature promoted the use of zinc in AD patients, a recent study has contradicted this and implicated zinc in the aetiology of Alzheimer's disease. On the basis of the above resutts, it may be premature to single out zinc as a causal agent in AD

The South African Society of Psychiatrists (SASOP) Treatment Guidelines for Psychiatric Disorders

CITATION: Emsely, R. et al. 2013. The South African Society of Psychiatrists (SASOP) treatment guidelines for psychiatric disorders. South African Journal of Psychiatry, 19(3):134-135, doi:10.4102/sajpsychiatry.v19i3.942.The original publication is available at http://www.sajp.org.zaThe South African Society of Psychiatrists (SASOP) Treatment Guidelines for Psychiatric Disorders have been developed in order to address the local need for guidelines in our unique clinical setting.http://www.sajp.org.za/index.php/sajp/article/view/942Publisher's versio