The symptomatology of Alzheimer's disease: a cross-cultural study

Karim, Salman; Minhas, Hassan M.; Bhattacharya, Sharmi; Sein, Kyaw; Nayar, Babu; Morris, Julie; Nizami, Asad Tamizuddin; Minhas, Fareed Aslam; Burns, Alistair

doi:10.1002/gps.2544

Cited by 6 publications

(3 citation statements)

References 36 publications

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“…The economic and social toll of AD is not restricted to patient care costs, but includes significant resource and emotional stress upon family members and other caregivers [1,3,4]. In addition to psychiatric symptoms such as memory loss, dementia, and depression [5][6][7] AD is characterized by intraneuronal aggregates of microtubule associated protein (gene name MAPT) [8] and extraneuronal plaques consisting of primarily amyloid - [9], with lesser proportions of inflammatory proteins (including vimentin), lytic proteins (including ATPase, H+ transporting, lysosomal 31kDa, V1 subunit E1), kinases (including tyrosine 3-monooxygenase), protein, and at least 21 additional peptides [10]. Other, non-amyloid, aggregates comprised mostly of -synuclein protein (gene name ASYN) may also play a role [11].…”

Section: Introduction Prevalence and Pathobiochemical Characteristicsmentioning

confidence: 99%

Applying Epigenetics to Alzheimer’s Disease via the Latent Early–life Associated Regulation (LEARn) Model

Maloney

Sambamurti

Zawia

et al. 2012

CAR

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Alzheimer's disease (AD) is a leading cause of aging related dementia and has been extensively studied by several groups around the world. A general consensus, based on neuropathology, genetics and cellular and animal models, is that the 4 kDa amyloid β protein (Aβ) triggers a toxic cascade that induces microtubule-associated protein τ (MAPT) hyperphosphorylation and deposition. Together, these lesions lead to neuronal dysfunction and neurodegeneration, modeled in animals, that ultimately causes dementia. Genetic studies show that a simple duplication of the Aβ precursor (APP) gene, as occurs in Down syndrome (trisomy 21), with a 1.5-fold increase in expression, can cause dementia with the complete AD associated neuropathology. The most fully characterized form of AD is early onset familial AD (FAD). Unfortunately, by far the most common form of AD is late onset AD (LOAD). FAD has well-identified autosomally dominant genetic causes, absent in LOAD. It is reasonable to hypothesize that environmental influences play a much stronger role in etiology of LOAD than of FAD. Since AD pathology in LOAD closely resembles FAD with accumulation of both Aβ and MAPT, it is likely that the environmental factors foster accumulation of these proteins in a manner similar to FAD mutations. Therefore, it is important to identify environmentally driven changes that "phenocopy" FAD in order to find ways to prevent LOAD. Epigenetic changes in expression are complex but stable determinants of many complex traits. Some aspects are regulated by prenatal and early post-natal development, others punctuate specific periods of maturation, and still others occur throughout life, mediating predictable changes that take place during various developmental stages. Environmental agents such as mercury, lead, and pesticides can disrupt the natural epigenetic program and lead to developmental deficits, mental retardation, feminization, and other complex syndromes. In this review we discuss latent early- life associated regulation (LEARn), where apparently temporary changes, induced by environmental agents, become latent and present themselves again at maturity or senescence to increase production of Aβ that may cause AD. The model provides us with a novel direction for identifying potentially harmful agents that may induce neurodegeneration and dementia later in life and provides hope that we may be able to prevent age-related neurodegenerative disease by "detoxifying" our environment.

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Section: Introduction Prevalence and Pathobiochemical Characteristicsmentioning

confidence: 99%

Applying Epigenetics to Alzheimer’s Disease via the Latent Early–life Associated Regulation (LEARn) Model

Maloney

Sambamurti

Zawia

et al. 2012

CAR

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“…All CALD participants immigrated to Australia during their lifetime, CALD-LOTE participants were fluent in their native language and in English at the time of initial assessment. Our approach was based on previous studies that categorised participants according to country of birth and first language to isolate the influence of culture and language upon cognitive and clinical symptoms [ 16 , 17 ]. All healthy controls were Australian and were selected from a larger control cohort and matched to the patient groups on sex (Table 1 for the cultural profile of each group).…”

Section: Methodsmentioning

confidence: 99%

The influence of culture and cognitive reserve on the clinical presentation of behavioural-variant frontotemporal dementia

et al. 2023

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Characterisation of the clinical profile of behavioural-variant frontotemporal dementia (bvFTD) has predominantly been based on Western samples. Some small studies have suggested that the clinical profile may differ in culturally and linguistically diverse populations. Additionally, there is evidence that patients from non-English speaking backgrounds may have more cognitive reserve, allowing them to tolerate more disease pathology before clinical symptoms emerge. This study aims to characterise the clinical profiles of patients with bvFTD from culturally diverse backgrounds. BvFTD patients were classified as Australian-born (Australian) or Culturally and Linguistically Diverse-English-speaking (CALD-English) and Culturally and Linguistically Diverse-Language Other Than English (CALD-LOTE). Clinical features, cognitive test performance and cognitive reserve were compared between groups. Voxel-based morphometry was used to examine the neural correlates of cognitive reserve. 107 patients with bvFTD (53 Australian, 36 CALD-English, 18 CALD-LOTE) and 51 controls were included. Analysis of neuropsychiatric features revealed more elation in Australian patients compared to CALD-English patients, with trends for CALD-LOTE patients to report more irritability. CALD-LOTE patients also had higher cognitive reserve and showed relatively greater verbal than non-verbal cognitive impairment. Neuroimaging analyses revealed that higher cognitive reserve was associated with lower integrity in the frontal–temporal regions associated with typical disease pathology in bvFTD. Our findings support the hypothesis that cognitive reserve may delay early cognitive decline in culturally and linguistically diverse patients, although these patients may still show poor verbal performance due to cultural testing biases. Clinically, these results highlight the need to consider cultural and linguistic background to inform the assessment of dementia.

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“…Research on cross‐cultural differences has grown in recent years, in general, and particularly in mental health (Jia et al , ; Karim et al , ). Understanding true racial/ethnic differences in the development and symptomatology of mental health problems, including depressive symptoms, requires first and foremost reliable and valid measures.…”

Section: Introductionmentioning

confidence: 99%

Comparisons of CES‐D depression scoring methods in two older adults ethnic groups. The emergence of an ethnic‐specific brief three‐item CES‐D scale

Coman

Iordache

Schensul

et al. 2012

Int J Geriat Psychiatry

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The symptomatology of Alzheimer's disease: a cross-cultural study

Cited by 6 publications

References 36 publications

Applying Epigenetics to Alzheimer’s Disease via the Latent Early–life Associated Regulation (LEARn) Model

Applying Epigenetics to Alzheimer’s Disease via the Latent Early–life Associated Regulation (LEARn) Model

The influence of culture and cognitive reserve on the clinical presentation of behavioural-variant frontotemporal dementia

Comparisons of CES‐D depression scoring methods in two older adults ethnic groups. The emergence of an ethnic‐specific brief three‐item CES‐D scale

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