Prevalence of dementia subtypes: A 30-year retrospective survey of neuropathological reports

Brunnström, Hans; Gustafson, Lars; Passant, Ulla; Englund, Elisabet

doi:10.1016/j.archger.2008.06.005

Cited by 131 publications

(96 citation statements)

References 26 publications

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“…Результаты патологанатомических исследований, проведенных в течение последних двух десятилетий, показывают, что амилоидные бляшки часто встречаются при ЦВЗ, а ЦВЗ в качестве сопутствующей патологии могут модулировать риск и выраженность клинических про-явлений деменции [2]. Нейропатологические исследо-вания свидетельствуют о том, что БА и ЦВЗ в качестве сопутствующих заболеваний, диагностируют у 6-47% лиц с деменцией (таблица) [3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20]. Действительно, в большинстве случаев причиной развития деменции является смешанная патология (38%).…”

Section: Infarcts and Amyloid Plaquesunclassified

“…2 Neuropathological examinations show that between 6% and 47% individuals with dementia had coexisting AD and CVD pathologies (Table). [3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20] Indeed, mixed pathologies may account for the majority of dementia cases (38%). 11 Although autopsy study is considered the gold standard for determining the underlying pathology of dementia, it has inherent limitations with correlating pathological and clinical findings.…”

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confidence: 99%

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Cerebrovascular Disease, Amyloid Plaques, and Dementia

Liu

Wong

Law

et al. 2015

Stroke

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Absence of vascular dementia in an autopsy series from a dementia clinic. J Am Geriatr Soc. 1998;46:597-604. 6. Seno H, Ishino H, Inagaki T, Iijima M, Kaku K, Inata T. A neuropathological study of dementia in nursing homes over a 17-year period, in Shimane Prefecture, Japan. Gerontology. 1999;45:44-48. 7 However, an unresolved issue remains on the temporal relationship between the development of vascular and amyloid pathologies as other potential factors, such as the overproduction of Aβ caused by genetic mutations in APP and presenilin genes might also take part in the abnormal amyloid accumulation. Atherosclerosis and Amyloid PlaquesAtherosclerosis in large cerebral arteries can compromise cerebral blood flow and cause cerebral hypoperfusion. Patients with AD had a higher proportion and more pronounced atherosclerosis in the circle of Willis than those patients with non-AD dementias (except VaD) as shown in autopsy studies. 41,[55][56][57][58] Moreover, there was a high concordance between the ratings of atherosclerosis with amyloid plaques and CAA ratings. 41Through [18F] AV-45 PET examination, amyloid deposition in patients with dementia having unilateral carotid artery stenosis was increased. More importantly, the distribution of the amyloid disposition was found to be lateralized to the side of stenosis.26 Together, these clinical and pathological findings suggest that there is a shared cause between atherosclerosis and amyloid deposition. Infarcts and Amyloid PlaquesMost amyloid PET studies did not find significant relationships between infarcts and amyloid deposition. 27,28 In fact, a study showed that in patients with subcortical vascular cognitive impairment, the number of lacunes was negatively related with the PiB retention ratio. 29 In patients with recent ischemic stroke, although a relatively increased PiB retention was found in peri-infarct region comparing to the contralateral mirror region, this increased regional PiB retention did not translate into a higher global PiB retention. 30 In experimental stroke models in transgenic mouse with amyloid deposition (APPswe/PS1dE9), increase in new amyloid plaques around the infarcted area was only transient, in which the accumulation most probably reflected an impaired amyloid clearance pathway caused by infarcted tissue. 59 Moreover, the possibility that the observed increase in local PiB retention being a result of leakage of free PiB because of the blood-brain barrier damage could not be excluded. 30 Overall, thus far, there is no solid evidence of a significant interaction between cerebral infarcts and global amyloid burden. Sources of Funding

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Section: Infarcts and Amyloid Plaquesunclassified

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confidence: 99%

Cerebrovascular Disease, Amyloid Plaques, and Dementia

Liu

Wong

Law

et al. 2015

Stroke

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“…Frontotemporal lobar degeneration (FTLD) is the second most prevalent dementia in patients below 65 years old1, 2 and has the worst life expectancy among non‐prion dementia 3. Two main pathological subtypes have been described based on the proteinopathy found in the brain: around half of the cases develop aggregates of the microtubule‐associated protein tau (FTLD‐Tau), while the other half are characterized by cytoplasmic inclusions of the transactivator regulatory DNA‐binding protein 43 (TDP43, FTLD‐TDP) 4.…”

Section: Introductionmentioning

confidence: 99%

Novel CSF biomarkers to discriminate FTLD and its pathological subtypes

Campo

Galimberti

Elias

et al. 2018

Ann Clin Transl Neurol

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ObjectiveFrontotemporal lobar degeneration (FTLD) is the second most prevalent dementia in young patients and is characterized by the presence of two main protein aggregates in the brain, tau (FTLD‐Tau) or TDP43 (FTLD‐TDP), which likely require distinct pharmacological therapy. However, specific diagnosis of FTLD and its subtypes remains challenging due to largely overlapping clinical phenotypes. Here, we aimed to assess the clinical performance of novel cerebrospinal fluid (CSF) biomarkers for discrimination of FTLD and its pathological subtypes.Methods YKL40, FABP4, MFG‐E8, and the activities of catalase and specific lysosomal enzymes were analyzed in patients with FTLD‐TDP (n = 30), FTLD‐Tau (n = 20), AD (n = 30), DLB (n = 29), and nondemented controls (n = 29) obtained from two different centers. Models were validated in an independent CSF cohort (n = 188).Results YKL40 and catalase activity were increased in FTLD‐TDP cases compared to controls. YKL40 levels were also higher in FTLD‐TDP compared to FTLD‐Tau. We identified biomarker models able to discriminate FTLD from nondemented controls (MFG‐E8, tTau, and Aβ 42; 78% sensitivity and 83% specificity) and non‐FTLD dementia (YKL40, pTau, p/tTau ratio, and age; 90% sensitivity, 78% specificity), which were validated in an independent cohort. In addition, we identified a biomarker model differentiating FTLD‐TDP from FTLD‐Tau (YKL40, MFGE‐8, βHexA together with βHexA/tHex and p/tTau ratios and age) with 80% sensitivity and 82% specificity.InterpretationThis study identifies CSF protein signatures distinguishing FTLD and the two main pathological subtypes with optimal accuracy (specificity/sensitivity > 80%). Validation of these models may allow appropriate selection of cases for clinical trials targeting the accumulation of Tau or TDP43, thereby increasing their efficiency and facilitating the development of successful therapies.

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“…Frontotemporal lobar degeneration (FTLD) is the second most common form of neurodegenerative dementia in the presenile population and the third most prevalent form of neurodegenerative dementia overall 1, 2. With an estimated prevalence of 15/100,000 in the age group of 45–64 years, FTLD represents a significant challenge for social welfare 1, 3.…”

Section: Introductionmentioning

confidence: 99%

Diagnostic utility of ASL‐MRI and FDG‐PET in the behavioral variant of FTD and AD

Tosun

Schuff

Rabinovici

et al. 2016

Ann Clin Transl Neurol

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ObjectiveTo compare the values of arterial spin‐labeled (ASL) MRI and fluorodeoxyglucose (FDG) PET in the diagnosis of behavioral variant of frontotemporal dementia (bvFTD) and Alzheimer's disease (AD).MethodsPartial least squares logistic regression was used to identify voxels with diagnostic value in cerebral blood flow (CBF) and cerebral metabolic rate of glucose (CMRgl) maps from patients with bvFTD (n = 32) and AD (n = 28), who were compared with each other and with cognitively normal controls (CN, n = 15). Diagnostic values of these maps were compared with each other.ResultsRegions that differentiated each disorder from controls were similar for CBF and CMRgl. For differentiating AD from CN, the areas under the curve (AUC) for CBF (0.89) and CMRgl (0.91) were similar, with similar sensitivity (CBF: 86%, CMRgl: 78%) and specificity (CBF: 92%, CMRgl: 100%). Likewise, for differentiating bvFTD from CN performances of CBF (AUC = 0.83) and CMRgl (AUC = 0.85) were equivalent, with similar sensitivity (CBF: 78%, CMRgl: 79%) and specificity (CBF: 92%, CMRgl: 100%). In differentiating bvFTD from AD, classification was again similar for CBF (AUC = 0.87) and CMRgl (AUC = 0.79), as were sensitivity (CBF: 83%, CMRgl: 89%) and specificity (CBF: 93%, CMRgl: 78%). None of the differences in any performance measure were statistically significant.InterpretationASL‐MRI has similar diagnostic utility as FDG‐PET in the diagnosis of AD and bvFTD. Continued development of ASL‐MRI as a diagnostic tool for neurodegenerative dementias is warranted.

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Prevalence of dementia subtypes: A 30-year retrospective survey of neuropathological reports

Cited by 131 publications

References 26 publications

Cerebrovascular Disease, Amyloid Plaques, and Dementia

Cerebrovascular Disease, Amyloid Plaques, and Dementia

Novel CSF biomarkers to discriminate FTLD and its pathological subtypes

Diagnostic utility of ASL‐MRI and FDG‐PET in the behavioral variant of FTD and AD

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