Profile of clinically-diagnosed dementias in a neuropsychiatric practice in Abeokuta, South-Western Nigeria

Objective: Many subjects with dementia present primarily to neuropsychiatric practices because of behavioural and psychological symptoms (BPSD). This study reviewed the profile of clinically-diagnosed dementias and BPSD seen in a pioneer neuropsychiatric practice in Abeokuta, southwestern Nigeria over a ten year period (January1998 – December 2007). Methods: A review of hospital records of all patients with diagnoses of dementia or dementing illness using the ICD-10 criteria as well as specific diagnostic criteria for different dementia phenotypes. Associated BPSD, co-morbidities and treatments were also reviewed. Results: Out of a total of 240,294 patients seen over the study period, 108 subjects met clinical diagnostic criteria for probable dementia giving a hospital frequency of 45 per 100,000. Alzheimer’s disease (AD) and Vascular dementia (VaD) were the predominant phenotypes seen in 62 (57.4%) and 18 (16.7%) subjects respectively. Others include mixed dementia (4 cases), frontotemporal dementia (4 cases), Lewy body dementia (3 cases), alcohol-related dementia (3 cases), PD dementia (1 case) and unclassifiable (13 cases). Apathy, night time behaviour, aberrant motor behaviour, agitation and irritability were the most common BPSD features, while hypertension was the most common co-morbidity. Neuroleptics, anticholinergics and anti-hypertensives were most commonly prescribed. Anticholinesterase inhibitors were sparingly used. Conclusion: Probable AD was the most prevalent dementia phenotype seen in this practice. Increased awareness of dementia and better utilization of specific treatments are needed among psychiatrists and primary care practitioners in Nigeria.Keywords: Dementia phenotypes; BPSD; Neuropsychiatric practice; Nigeria; Afric

Current perspectives on prevention of vascular cognitive impairment and promotion of vascular brain health

\ua9 2023 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. Introduction: The true global burden of vascular cognitive impairment (VCI) is unknown. Reducing risk factors for stroke and cardiovascular disease would inevitably curtail VCI. Areas Covered: The authors review current diagnosis, epidemiology, and risk factors for VCI. VCI increases in older age and by inheritance of known genetic traits. They emphasize modifiable risk factors identified by the 2020 Lancet Dementia Commission. The most profound risks for VCI also include lower education, cardiometabolic factors, and compromised cognitive reserve. Finally, they discuss pharmacological and non-pharmacological interventions. Expert Opinion: By virtue of the high frequencies of stroke and cardiovascular disease the global prevalence of VCI is expectedly higher than prevalent neurodegenerative disorders causing dementia. Since ~ 90% of the global burden of stroke can be attributed to modifiable risk factors, a formidable opportunity arises to reduce the burden of not only stroke but VCI outcomes including progression from mild to the major in form of vascular dementia. Strict control of vascular risk factors and secondary prevention of cerebrovascular disease via pharmacological interventions will impact on burden of VCI. Non-pharmacological measures by adopting healthy diets and encouraging physical and cognitive activities and urging multidomain approaches are important for prevention of VCI and preservation of vascular brain health

Frontal white matter hyperintensities, clasmatodendrosis and gliovascular abnormalities in ageing and post-stroke dementia

White matter hyperintensities as seen on brain T2-weighted magnetic resonance imaging are associated with varying degrees of cognitive dysfunction in stroke, cerebral small vessel disease and dementia. The pathophysiological mechanisms within the white matter accounting for cognitive dysfunction remain unclear. With the hypothesis that gliovascular interactions are impaired in subjects with high burdens of white matter hyperintensities, we performed clinicopathological studies in post-stroke survivors, who had exhibited greater frontal white matter hyperintensities volumes that predicted shorter time to dementia onset. Histopathological methods were used to identify substrates in the white matter that would distinguish post-stroke demented from post-stroke non-demented subjects. We focused on the reactive cell marker glial fibrillary acidic protein (GFAP) to study the incidence and location of clasmatodendrosis, a morphological attribute of irreversibly injured astrocytes. In contrast to normal appearing GFAP + astrocytes, clasmatodendrocytes were swollen and had vacuolated cell bodies. Other markers such as aldehydedehydrogenase 1 family, member L1 (ALDH1L1) showed cytoplasmic disintegration of the astrocytes. Total GFAP + cells in both the frontal and temporal white matter were not greater in post-stroke demented versus post-stroke non-demented subjects. However, the percentage of clasmatodendrocytes was increased by 42-fold in subjects with post-stroke demented compared to post-stroke non-demented subjects (P = 0.026) and by 11-fold in older controls versus young controls (P50.023) in the frontal white matter. High ratios of clasmotodendrocytes to total astrocytes in the frontal white matter were consistent with lower Mini-Mental State Examination and the revised Cambridge Cognition Examination scores in post-stroke demented subjects. Double immunofluorescent staining showed aberrant co-localization of aquaporin 4 (AQP4) in retracted GFAP + astrocytes with disrupted end-feet juxtaposed to microvessels. To explore whether this was associated with the disrupted gliovascular interactions or blood–brain barrier damage, we assessed the co-localization of GFAP and AQP4 immunoreactivities in post-mortem brains from adult baboons with cerebral hypoperfusive injury, induced by occlusion of three major vessels supplying blood to the brain. Analysis of the frontal white matter in perfused brains from the animals surviving 1–28 days after occlusion revealed that the highest intensity of fibrinogen immunoreactivity was at 14 days. At this survival time point, we also noted strikingly similar redistribution of AQP4 and GFAP + astrocytes transformed into clasmatodendrocytes. Our findings suggest novel associations between irreversible astrocyte injury and disruption of gliovascular interactions at the blood–brain barrier in the frontal white matter and cognitive impairment in elderly post-stroke survivors. We propose that clasmatodendrosis is another pathological substrate, linked to white matter hyperintensities and frontal white matter changes, which may contribute to post-stroke or small vessel disease dementia

Non-Communicable Neurological Disorders and Neuroinflammation

Copyright \ua9 2022 Ballerini, Njamnshi, Juliano, Kalaria, Furlan and Akinyemi. Traumatic brain injury, stroke, and neurodegenerative diseases represent a major cause of morbidity and mortality in Africa, as in the rest of the world. Traumatic brain and spinal cord injuries specifically represent a leading cause of disability in the younger population. Stroke and neurodegenerative disorders predominantly target the elderly and are a major concern in Africa, since their rate of increase among the ageing is the fastest in the world. Neuroimmunology is usually not associated with non-communicable neurological disorders, as the role of neuroinflammation is not often considered when evaluating their cause and pathogenesis. However, substantial evidence indicates that neuroinflammation is extremely relevant in determining the consequences of non-communicable neurological disorders, both for its protective abilities as well as for its destructive capacity. We review here current knowledge on the contribution of neuroinflammation and neuroimmunology to the pathogenesis of traumatic injuries, stroke and neurodegenerative diseases, with a particular focus on problems that are already a major issue in Africa, like traumatic brain injury, and on emerging disorders such as dementias

Geo-demographic and socioeconomic determinants of diagnosed hypertension among urban dwellers in Ibadan, Nigeria: a community-based study

\ua9 The Author(s) 2024. Background: The relationship between diagnosed high blood pressure (HBP) and proximity to health facilities and noise sources is poorly understood. We investigated the associations between the number of persons diagnosed with HBP at different distance corridors of noise-generating sources (churches, mosques, bus stops, and road networks), and blood pressure monitoring outlets (healthcare facilities and pharmaceutical shops) in Ibadan, Nigeria. In addition, we investigated the likelihood of being diagnosed with HBP using distance from noise-generating sources, distance to blood pressure monitoring outlets, socio-demographic and clinical status of the participants. Methods: We investigated 13,531 adults from the African Rigorous Innovative Stroke Epidemiological Surveillance (ARISES) study in Ibadan. Using a Geographic Information System (GIS), the locations of healthcare facilities, pharmaceutical shops, bus stops, churches, and mosques were buffered at 100 m intervals, and coordinates of persons diagnosed with HBP were overlaid on the buffered features. The number of persons with diagnosed HBP living at every 100 m interval was estimated. Gender, occupation, marital status, educational status, type of housing, age, and income were used as predictor variables. Analysis was conducted using Spearman rank correlation and binary logistic regression at p < 0.05. Results: There was a significant inverse relationship between the number of persons diagnosed with HBP and distance from pharmaceutical shops (r=-0.818), churches (r=-0.818), mosques (r=-0.893) and major roads (r= -0.667). The odds of HBP were higher among the unemployed (AOR = 1.58, 95% CI: 1.11–2.24), currently married (AOR = 1.45, CI: 1.11–1.89), and previously married (1.75, CI: 1.29–2.38). The odds of diagnosed HBP increased with educational level and age group. Conclusion: Proximity to noise sources, being unemployed and educational level were associated with diagnosed HBP. Reduction in noise generation, transmission, and exposure could reduce the burden of hypertension in urban settings

Geo-behavioural predictors of diagnosed hypertension in Igbo Ora Area, Oyo State, Nigeria

\ua9 The Author(s) 2025.Diagnosed hypertension stands out as a prominent global cause of mortality, prompting recent efforts to understand not only treatment options but also determinants across diverse age and occupational groups. However, the literature on the impact of environmental factors on diagnosed hypertension is limited, especially in rural areas with restricted access to health infrastructure. Geographical determinants research has often focused on spatial variations across different units, potentially masking individual environmental contributions. Data on diagnosed hypertension patients and their behaviours were gathered during the ARISE project, complemented by geographical data (elevation, vegetation, road network, population density, and nighttime light exposure) from secondary sources. Spatial patterns were analyzed using the Nearest Neighbour Statistic, Ripley K Function, and Kernel Density Estimation, while Binomial logistic regression identified predictors. Diagnosed hypertension patients exhibit spatial clustering, and are mainly comprised of elderly individuals, residing closer to roads, at higher elevations, in areas with higher population distribution, and with little or no green vegetation. Socio-economic, health-related, behavioural, and environmental factors collectively drive diagnosed hypertension. Spatial clustering of diagnosed hypertension in the Igbo Ora community is localized, indicating potential spatial factors influencing its prevalence. Beyond identified behavioural and medical history factors, geographical elements like nighttime light exposure and normalized vegetation index contribute to the observed clustering. Understanding these dynamics is crucial for targeted interventions in the community

Global, regional, and national burden of neurological disorders during 1990-2015: a systematic analysis for the Global Burden of Disease Study 2015

Background Comparable data on the global and country-specific burden of neurological disorders and their trends are crucial for health-care planning and resource allocation. The Global Burden of Diseases, Injuries, and Risk Factors (GBD) Study provides such information but does not routinely aggregate results that are of interest to clinicians specialising in neurological conditions. In this systematic analysis, we quantified the global disease burden due to neurological disorders in 2015 and its relationship with country development level. Methods We estimated global and country-specific prevalence, mortality, disability-adjusted life-years (DALYs), years of life lost (YLLs), and years lived with disability (YLDs) for various neurological disorders that in the GBD classification have been previously spread across multiple disease groupings. The more inclusive grouping of neurological disorders included stroke, meningitis, encephalitis, tetanus, Alzheimer's disease and other dementias, Parkinson's disease, epilepsy, multiple sclerosis, motor neuron disease, migraine, tension-type headache, medication overuse headache, brain and nervous system cancers, and a residual category of other neurological disorders. We also analysed results based on the Socio-demographic Index (SDI), a compound measure of income per capita, education, and fertility, to identify patterns associated with development and how countries fare against expected outcomes relative to their level of development. Findings Neurological disorders ranked as the leading cause group of DALYs in 2015 (250·7 [95% uncertainty interval (UI) 229·1 to 274·7] million, comprising 10·2% of global DALYs) and the second-leading cause group of deaths (9·4 [9·1 to 9·7] million], comprising 16·8% of global deaths). The most prevalent neurological disorders were tension-type headache (1505·9 [UI 1337·3 to 1681·6 million cases]), migraine (958·8 [872·1 to 1055·6] million), medication overuse headache (58·5 [50·8 to 67·4 million]), and Alzheimer's disease and other dementias (46·0 [40·2 to 52·7 million]). Between 1990 and 2015, the number of deaths from neurological disorders increased by 36·7%, and the number of DALYs by 7·4%. These increases occurred despite decreases in age-standardised rates of death and DALYs of 26·1% and 29·7%, respectively; stroke and communicable neurological disorders were responsible for most of these decreases. Communicable neurological disorders were the largest cause of DALYs in countries with low SDI. Stroke rates were highest at middle levels of SDI and lowest at the highest SDI. Most of the changes in DALY rates of neurological disorders with development were driven by changes in YLLs. Interpretation Neurological disorders are an important cause of disability and death worldwide. Globally, the burden of neurological disorders has increased substantially over the past 25 years because of expanding population numbers and ageing, despite substantial decreases in mortality rates from stroke and communicable neurological disorders. The number of patients who will need care by clinicians with expertise in neurological conditions will continue to grow in coming decades. Policy makers and health-care providers should be aware of these trends to provide adequate services

Genetic architecture of Alzheimer’s disease in a West African Cohort: Insights from the READD - ADSP

\ua9 2024 The Alzheimer\u27s Association. Alzheimer\u27s & Dementia published by Wiley Periodicals LLC on behalf of Alzheimer\u27s Association. BACKGROUND: The "Recruitment and Retention for Alzheimer\u27s Disease Diversity Genetic Cohorts in the ADSP (READD-ADSP)" is developing a resource to expand ancestral diversity in Alzheimer disease (AD) studies to dissect the genetic architecture of AD across different populations. In addition to US sites, READD-ADSP includes four US sites and nine countries in sub-Saharan Africa through the Africa Dementia Consortium (AfDC). The overall goal of READD-ADSP is to identify genetically driven targets in diverse groups including African Americans and Hispanic/Latinos in US, and Africans. In this preliminary analysis we investigated the ancestral genetic differences and the impact of known AD risk factors within West African cohorts. METHOD: Genome-wide genotyping was performed on 91 AD cases and 97 cognitive unimpaired controls from Nigeria and Ghana. APOE alleles and ABCA7 deletion (rs142076058) were sequenced using Sanger. We calculated global ancestry (principal components) using the PC-AiR approach that is robust to known and cryptic relatedness. We investigated known AD loci from non-Hispanic White (NHW) and AA genome wide association studies. For association analysis, we employed a mixed-model regression approach (SAIGE) where we controlled for age, gender, population substructure (first three principal components), and relatedness. RESULT: Principal component analysis identified a distinction between the Ghana and Nigerian cohorts along the first principal component (PC1). Among the genetic loci examined, several showed nominal significance. Notably, the most prominent marker was found in SORL1 (rs17125523; p = 2 7 10-3). Additionally, we discovered an exonic nonsynonymous marker in the BIN1 gene (rs112318500), which is specific to African ancestry and showed a protective effect. APOE e4 allele showed a significant association with AD risk (OR = 2.5; CI:1.5-4.2; pv = 0.001), while the e2 indicated a protective trend but did not reach statistical significance. No statistical difference in the frequency of ABCA7 deletion was observed between AD and CU individuals. CONCLUSION: Our findings highlight the presence of genetic variations between West African populations that warrant further investigation, potentially offering new insights into the genetic underpinnings of AD. Data collection is ongoing across the AfDC and updated data will be presented