Frequency of Alzheimer's Disease and Other Dementias in a Community Outreach Sample of Hispanics

Fitten, L. Jaime; Ortiz, Freddy; Pontón, Marcel O.

doi:10.1046/j.1532-5415.2001.49257.x

Cited by 95 publications

(87 citation statements)

References 46 publications

(48 reference statements)

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“…Only two studies to date have reported cases of non-AD and non-VaD dementias in diverse ethnic populations in the USA [2,6] . PSP was diagnosed in 6 JapaneseAmerican men with dementia [2] .…”

Section: Discussionmentioning

confidence: 99%

“…PSP was diagnosed in 6 JapaneseAmerican men with dementia [2] . Among a group of community-dwelling Latinos, FTLD was the third most common cause of dementia, accounting for 6 cases or 9.2% of the sample [6] . This frequency is higher than the 2.4% of Latinos with a diagnosis of FTLD in this study.…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies have investigated the rates of non-AD and non-VaD dementia subtypes in various community samples [6,[15][16][17] . AD and FTLD were diagnosed in an equal number of cases (15.1%) of early-onset dementia [16] .…”

Section: Discussionmentioning

confidence: 99%

“…The frequency of vascular dementia (VaD) was higher among Asians, Blacks and Latinos [2,5,6] . However, research on dementia among diverse commu-nities has focused primarily on AD and VaD.…”

Section: Introductionmentioning

confidence: 99%

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Frequency of Dementia Etiologies in Four Ethnic Groups

Hou

Yaffe²,

Pérez‐Stable³

et al. 2006

Dement Geriatr Cogn Disord

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Background/Aims: Research on dementia among ethnically diverse populations in the USA has focused primarily on Alzheimer disease and vascular dementia, but there are limited data on other neurodegenerative causes of dementia. Methods: To determine the frequency of neurodegenerative disorders in four ethnic groups, data collected at Alzheimer’s Disease Research Centers of California for assessments between 1992 and 2002 were analyzed retrospectively. Cases of Alzheimer disease, vascular dementia, dementia with Lewy bodies, frontotemporal lobar degeneration, Parkinson disease and progressive supranuclear palsy were identified for 452 Asian and Pacific Islander, 472 Black, 675 Latino and 4,926 White patients. Results: The percentage of non-Whites diagnosed as having dementia with Lewy bodies was lower than that of Whites. Frontotemporal lobar degeneration was as common in Asians and Pacific Islanders compared to Whites, but less common in Blacks and Latinos. Progressive supranuclear palsy was more frequent in Asians and Pacific Islanders compared to Whites, but equally common in Blacks and Latinos. Conclusion: Additional study is needed on the social and biological factors that influence the diagnosis and prevalence of non-Alzheimer and nonvascular dementias among diverse ethnic groups.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Frequency of Dementia Etiologies in Four Ethnic Groups

Hou

Yaffe²,

Pérez‐Stable³

et al. 2006

Dement Geriatr Cogn Disord

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“…The accumulation of insoluble amyloid "plaques" and oligomers of beta amyloid peptide (Ab) in the brain plays an important role in Alzheimer's disease (AD), which is one of the principal causes of dementia worldwide, 1 causing oxidative stress and inflammation in specific areas of the brain. 2 Amyloid fibrils and oligomers are formed by a process called amyloidosis, in which the beta-amyloid peptide (Ab) produces insoluble aggregates.…”

Section: Introductionmentioning

confidence: 99%

In silico and in vitro studies to elucidate the role of Cu²⁺ and galanthamine as the limiting step in the amyloid beta (1–42) fibrillation process

et al. 2013

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The formation of fibrils and oligomers of amyloid beta (Aβ) with 42 amino acid residues (Aβ1–42) is the most important pathophysiological event associated with Alzheimer's disease (AD). The formation of Aβ fibrils and oligomers requires a conformational change from an α‐helix to a β‐sheet conformation, which is encouraged by the formation of a salt bridge between Asp 23 or Glu 22 and Lys 28. Recently, Cu2+ and various drugs used for AD treatment, such as galanthamine (Reminyl®), have been reported to inhibit the formation of Aβ fibrils. However, the mechanism of this inhibition remains unclear. Therefore, the aim of this work was to explore how Cu2+ and galanthamine prevent the formation of Aβ1–42 fibrils using molecular dynamics (MD) simulations (20 ns) and in vitro studies using fluorescence and circular dichroism (CD) spectroscopies. The MD simulations revealed that Aβ1–42 acquires a characteristic U‐shape before the α‐helix to β‐sheet conformational change. The formation of a salt bridge between Asp 23 and Lys 28 was also observed beginning at 5 ns. However, the MD simulations of Aβ1−42 in the presence of Cu2+ or galanthamine demonstrated that both ligands prevent the formation of the salt bridge by either binding to Glu 22 and Asp 23 (Cu2+) or to Lys 28 (galanthamine), which prevents Aβ1−42 from adopting the U‐characteristic conformation that allows the amino acids to transition to a β‐sheet conformation. The docking results revealed that the conformation obtained by the MD simulation of a monomer from the 1Z0Q structure can form similar interactions to those obtained from the 2BGE structure in the oligomers. The in vitro studies demonstrated that Aβ remains in an unfolded conformation when Cu2+ and galanthamine are used. Then, ligands that bind Asp 23 or Glu 22 and Lys 28 could therefore be used to prevent β turn formation and, consequently, the formation of Aβ fibrils.

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Clinical Predictors of Severe Cerebral Amyloid Angiopathy and Influence ofAPOEGenotype in Persons With Pathologically Verified Alzheimer Disease

et al. 2014

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IMPORTANCE Although cerebral amyloid angiopathy (CAA) has important clinical implications, our understanding of it and ability to diagnose it are limited.OBJECTIVE To determine pathological correlates and clinical factors identifiable during life that predict the presence of severe CAA in persons with pathologically confirmed Alzheimer disease (AD). DESIGN, SETTING, AND PARTICIPANTSWe compared demographic and clinical variables at the earliest visit during life at which participants were found to have cognitive impairment and compared pathological variables between persons ultimately found to have no or severe CAA at autopsy using logistic regression. Analyses were repeated separately for carriers and noncarriers of the APOE ε4 allele. Data were obtained from the Uniform Data Set, which comprises longitudinal clinical assessments performed in the Alzheimer's Disease Centers funded by the National Institute on Aging. Participants included 193 persons with AD and severe CAA and 232 persons with AD and no CAA. All participants had cognitive impairment and met National Institute on Aging-Reagan Institute neuropathological criteria for AD. MAIN OUTCOMES AND MEASURESPrevalence of demographic characteristics and the APOE ε4 allele and odds ratios (ORs) of clinical variables for the prediction of severe CAA. RESULTSPersons with severe CAA compared with those without CAA were more likely to carry an APOE ε4 allele (64.9% vs 42.8%, respectively; P < .001), to be Hispanic (6.8% vs 1.3%, respectively; P = .003), to have had a transient ischemic attack (12.5% vs 6.1%, respectively; OR = 2.1; 95% CI, 1.0-4.4), and to have lower degrees of diffuse amyloid plaque pathology (mean [SD] Consortium to Establish a Registry for Alzheimer's Disease score, 1.2 [0.5] vs 1.4 [0.8], respectively; P = .01). Those with CAA compared with those without CAA more commonly had intracerebral hemorrhage (9.3% vs 3.5%, respectively; P = .01), cortical microinfarcts (20.7% vs 12.9%, respectively; P = .03), and subcortical leukoencephalopathy (20.5% vs 12.1%, respectively; P = .02). Noncarriers of the APOE ε4 allele with severe CAA compared with those without CAA had a higher prevalence of stroke (11.1% vs 3.9%, respectively; OR = 3.8; 95% CI, 1.0-14.6) and hypercholesterolemia (50.0% vs 32.7%, respectively; OR = 2.3; 95% CI, 1.1-4.7). CONCLUSIONS AND RELEVANCEBeing Hispanic and having had a transient ischemic attack-like episode were predictors of CAA in persons with AD. Less diffuse parenchymal amyloid pathology in persons with severe CAA suggests a difference in β-amyloid trafficking.

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Frequency of Alzheimer's Disease and Other Dementias in a Community Outreach Sample of Hispanics

Cited by 95 publications

References 46 publications

Frequency of Dementia Etiologies in Four Ethnic Groups

Frequency of Dementia Etiologies in Four Ethnic Groups

In silico and in vitro studies to elucidate the role of Cu²⁺ and galanthamine as the limiting step in the amyloid beta (1–42) fibrillation process

Clinical Predictors of Severe Cerebral Amyloid Angiopathy and Influence ofAPOEGenotype in Persons With Pathologically Verified Alzheimer Disease

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Frequency of Alzheimer's Disease and Other Dementias in a Community Outreach Sample of Hispanics

Cited by 95 publications

References 46 publications

Frequency of Dementia Etiologies in Four Ethnic Groups

Frequency of Dementia Etiologies in Four Ethnic Groups

In silico and in vitro studies to elucidate the role of Cu2+ and galanthamine as the limiting step in the amyloid beta (1–42) fibrillation process

Clinical Predictors of Severe Cerebral Amyloid Angiopathy and Influence ofAPOEGenotype in Persons With Pathologically Verified Alzheimer Disease

Contact Info

Product

Resources

About

In silico and in vitro studies to elucidate the role of Cu²⁺ and galanthamine as the limiting step in the amyloid beta (1–42) fibrillation process