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Cited by 852Dementia and Cognitive Impairment ResearchNeurological Disease Mechanisms and TreatmentsHistorical and Modern Theater Studies

Diagnostic Criteria for Vascular Cognitive Disorders: A VASCOG Statement

Open access
Sachdev, Perminder, Kalaria, Raj, O’Brien, John, Skoog, Ingmar, Alladi, Suvarna, Black, Sandra E., Blacker, Deborah, Blazer, Dan G. +11 more·2014·Alzheimer Disease & Associated Disorders
DOI 10.1097/wad.0000000000000034PMC PMC4139434
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Abstract

BACKGROUND: Several sets of diagnostic criteria have been published for vascular dementia since the 1960s. The continuing ambiguity in vascular dementia definition warrants a critical reexamination. METHODS: Participants at a special symposium of the International Society for Vascular Behavioral and Cognitive Disorders (VASCOG) in 2009 critiqued the current criteria. They drafted a proposal for a new set of criteria, later reviewed through multiple drafts by the group, including additional experts and the members of the Neurocognitive Disorders Work Group of the fifth revision of Diagnostic and Statistical Manual (DSM-5) Task Force. RESULTS: Cognitive disorders of vascular etiology are a heterogeneous group of disorders with diverse pathologies and clinical manifestations, discussed broadly under the rubric of vascular cognitive disorders (VCD). The continuum of vascular cognitive impairment is recognized by the categories of Mild Vascular Cognitive Disorder, and Vascular Dementia or Major Vascular Cognitive Disorder. Diagnostic thresholds are defined. Clinical and neuroimaging criteria are proposed for establishing vascular etiology. Subtypes of VCD are described, and the frequent cooccurrence of Alzheimer disease pathology emphasized. CONCLUSIONS: The proposed criteria for VCD provide a coherent approach to the diagnosis of this diverse group of disorders, with a view to stimulating clinical and pathologic validation studies. These criteria can be harmonized with the DSM-5 criteria such that an international consensus on the criteria for VCD may be achieved.

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Crossref · 10.1097/wad.0000000000000034

Cites

81 of 81 references verified0 citation errors · 0 not checkable

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Claims the paper makes

0 of 69 cited sources checked · 0 supported · 0 flagged

  • Interpretationnone given

    DTI abnormalities are not delineated well enough at present to be incorporated into diagnostic criteria.

    “Abnormalities on DTI are, however, not delineated well enough at present to be incorporated into diagnostic criteria.”
    Quote in the paperSubstantial claim
  • Premisecitation

    The preponderance of cognitive disturbance in vascular cognitive disorders is in processing speed and frontal-executive functions, manifesting as slowed information processing, poorer working memory, and reduced set-shifting.

    “A considerable body of literature has concluded that the preponderance of disturbance in vascular cognitive disorders is in processing speed and frontal-executive functions, manifesting as slowed information processing, poorer working memory and reduced set-shifting ability.10,14”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [10] Hachinski V Iadecola C Petersen RC National Institute of Neurological disorders and Stroke - Canadian Stroke Network Vascular Cognitive Impairment Harmonization Standards Stroke 2006 37 2220 2241 16917086 source

      Not checked in the free run.

    • cites [14] Looi JCL Sachdev PS Differentiation of vascular dementia from AD on neuropsychological tests Neurology 1999 53 670 678 10489025 source

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  • Premisecitation

    Evidence from clinical and pathological data suggests that the majority of WMLs in the brains of older people are ischemic in origin.

    “While the differential diagnosis is long, there is evidence from clinical and pathological data to suggest that the majority of these lesions in the brains of older people are ischemic in origin.51”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [51] Pantoni L Garcia JH Pathogenesis of leukoaraiosis: a review Stroke 1997 28 652 659 9056627 source

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  • Premisecitation

    The severity of cognitive deficits after subarachnoid hemorrhage is related to the severity of the hemorrhage.

    “their severity is related to the severity of SAH,62”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [62] Hunt WE Clinical assessment of SAH J Neurosurg 1983 59 550 551 6886772 source

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  • Premisecitation

    Cognitive impairment in VCD lies on a continuum from normal functioning to dementia.

    “The concept of VCI recognizes that cognitive impairment in VCD is on a continuum from normal functioning to dementia.12”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [12] Hachinski VC Bowler JV Vascular dementia Neurology 1993 43 2159 2160 8414002 source

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  • May combine two claims. 18
  • Classified as probably not a substantial claim. 6

  • May combine two claims.

    Premisecitation

    Evidence for significant vascular pathology in the brain usually relies on CT or structural MRI, with MRI being more sensitive, especially if standardized protocols are followed.

    “Evidence for significant vascular pathology in the brain usually relies on computed tomography (CT) or structural magnetic resonance imaging (MRI), with the latter being more sensitive, especially if the standardized protocols recommended by the harmonization group are followed.10”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [10] Hachinski V Iadecola C Petersen RC National Institute of Neurological disorders and Stroke - Canadian Stroke Network Vascular Cognitive Impairment Harmonization Standards Stroke 2006 37 2220 2241 16917086 source

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  • May combine two claims.

    Premisecitation

    Vascular and neurodegenerative processes may interact, so risk factors for cerebrovascular disease also increase the risk of AD.

    “Furthermore, there is increasing recognition that vascular and neurodegenerative processes may interact, so that risk factors for CVD also increase the risk of AD.20”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [20] Skoog I Vascular aspects in Alzheimer's disease J Neural Transm Suppl 2000 59 37 43 10961416 source

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  • May combine two claims.

    Premisereasoning

    Vascular cognitive disorders are a heterogeneous group with varied pathologies and clinical presentations.

    “Cognitive disorders of vascular etiology are a heterogeneous group of disorders with diverse pathologies and clinical manifestations, discussed broadly under the rubric of vascular cognitive disorders (VCD).”
    • Also stated in: § 3.1. Criteria for vascular cognitive disorders (VCD) · plain
      “The heterogeneity stems from the type of vascular lesion and the nature, extent and location of parenchymal injury.”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites [5] Chui HC Victoroff JI Margolin D Criteria for the diagnosis of ischemic vascular dementia proposed by the State of California Alzheimer’s Disease Diagnostic and Treatment Centers Neurology 1992 42 473 480 1549205 source

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    • cites [10] Hachinski V Iadecola C Petersen RC National Institute of Neurological disorders and Stroke - Canadian Stroke Network Vascular Cognitive Impairment Harmonization Standards Stroke 2006 37 2220 2241 16917086 source

      Not checked in the free run.

    • cites [17] Jellinger KA Morphologic diagnosis of "vascular dementia" - a critical update J Neurol Sci 2008 270 1 12 18455191 source

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  • May combine two claims.

    Premisecitation

    Vascular brain damage can exist without evident cognitive impairment, and such asymptomatic individuals may be at increased risk of future decline.

    “Vascular brain damage can exist without any evident cognitive impairment, and such asymtomatic individuals may be at an increased risk of future decline and are worthy of medical attention to prevent such decline.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [12] Hachinski VC Bowler JV Vascular dementia Neurology 1993 43 2159 2160 8414002 source

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  • May combine two claims.

    Premisecitation

    VaD is not a single disease but has diverse etiologies, only some of which have well-characterized clinical manifestations.

    “Fifth, VaD is not one disease but rather has diverse etiologies, only some of which have well-characterized clinical manifestations.17”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [17] Jellinger KA Morphologic diagnosis of "vascular dementia" - a critical update J Neurol Sci 2008 270 1 12 18455191

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    Premisecitation

    The commonly used VaD criteria sets differ substantially in their requirements, so prevalence estimates can vary by many orders of magnitude when applied to the same dataset.

    “Fourth, the criteria sets differ significantly on the requirements for levels of cognitive impairment, number and location of strokes, neuroimaging abnormalities and neurological features, such that when applied to the same data set, the prevalence estimates can vary by many orders of magnitude.15,16”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [15] Wetterling T Kanitz RD Borgis KJ Comparison of different diagnostic criteria for vascular dementia (ADDTC, DSM-IV, ICD-10, NINDS-AIREN) Stroke 1996 27 30 36 8553399 source

      Not checked in the free run.

    • cites [16] Pohjasvaara T Erkinjuntti T Vataja R Dementia three months after stroke. Baseline frequency and effect of different definitions of dementia in the Helsinki Stroke Aging Memory Study (SAM) cohort Stroke 1997 28 785 792 9099197 source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Study design and conductreasoning

    The proposed criteria were developed through a VASCOG symposium, multiple drafts, additional experts, and review by the DSM-5 Neurocognitive Disorders Work Group.

    “Participants at a special symposium of the International Society for Vascular Behavioral and Cognitive Disorders (VASCOG) in 2009 critiqued the current criteria. They drafted a proposal for a new set of criteria, later reviewed through multiple drafts by the group, including additional experts and the members of the Neurocognitive Disorders Work Group of the DSM-5 Task Force.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Premisecitation

    Demonstration of abnormalities on neuroimaging is critical for increased certainty in diagnosis, and lack of neuroimaging data can cause significant diagnostic inaccuracy by overlooking silent brain infarction and WMLs.

    “The demonstration of abnormalities on neuroimaging is critical for increased certainty in the diagnosis, and the lack of neuroimaging data can result in significant diagnostic inaccuracy by overlooking silent brain infarction and WMLs.37”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [37] Tullberg M Fletcher E DeCarli C White matter lesions impair frontal lobe function regardless of their location Neurology 2004 63 246 253 15277616 PMC1893004 source

      Not checked in the free run.

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    Premisecitation

    WMLs are highly prevalent in the brains of elderly and even middle-aged individuals, and the lesions must be extensive to be clinically significant.

    “WMLs are highly prevalent in the brains of elderly and even middle-aged individuals,54,55 and the lesions have to be extensive to be clinically significant.”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [54] Wen W Sachdev P The topography of white matter hyperintensities on brain MRI in healthy 60- to 64-year old individuals Neuroimage 2004 22 144 154 15110004 source

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    • cites [55] Wen W Sachdev P Li JJ White matter hyperintensities in the forties: Their prevalence and topography in an epidemiological sample aged 44–48 Hum Brain Mapp 2009 30 1155 1167 18465744 PMC6870596 source

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  • May combine two claims.

    Premisecitation

    Many older people with dementia have combined vascular and Alzheimer-type pathology, and the two pathologies have an additive effect on cognition.

    “many older individuals with dementia suffer from a combination of vascular and Alzheimer-type pathology with an additive effect on cognition,19”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [19] Snowdon DA Greiner LH Mortimer JA Brain infarction and the clinical expression of Alzheimer’s disease: The nun study JAMA 1997 227 813 817 9052711 source

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  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Cognitive deficits occur in 19-62% of patients after subarachnoid hemorrhage.

    “Cognitive deficits have been reported in 19–62% of patients following SAH,61”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [61] Starkstein SE Jorge R Capizzano AA Uncommon causes of cerebrovascular dementia Int Psychogeriatr 2005 17 S51 S64 16240483 source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductown data

    The criteria were discussed at the 5th and 6th VASCOG conferences before being finalized.

    “The criteria were discussed at the 5th VASCOG conference in September 2011 in Lille, France and the 6th VASCOG conference in June 2013 in Toronto, Canada before being finalized.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    VaD is generally regarded as the second most common single cause of dementia after AD.

    “while VaD is generally regarded as the second most common single cause of dementia after AD,18”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [18] Fratiglioni L Launer LJ Andersen K Incidence of dementia and major subtypes in Europe: A collaborative study of population-based cohorts. Neurologic Diseases in the Elderly Research Group Neurology 2000 54 S10 S15 10854355

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  • May combine two claims.

    Premisecitation

    In subarachnoid hemorrhage, older age, arterial vasospasm, delayed cerebral infarction, raised intracranial pressure, intraparenchymal and intraventricular hemorrhage, hydrocephalus, and aneurysm location are important factors for cognitive deficits.

    “although other factors such as older age, the presence of arterial vasospasm and delayed cerebral infarction, increased intracranial pressure, intraparenchymal and intraventricular hemorrhages, hydrocephalus, and location of the aneurysm are all important.61”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [61] Starkstein SE Jorge R Capizzano AA Uncommon causes of cerebrovascular dementia Int Psychogeriatr 2005 17 S51 S64 16240483 source

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  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Amyloid imaging with radiolabeled Pittsburgh compound B has been proposed as a biomarker of Alzheimer's disease.

    “More recently, the imaging of amyloid with compounds such as the radiolabeled Pittsburgh compound B (11C-PiB) has received much interest and been proposed as a biomarker of AD.21,22”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [21] McKhann GM Knopman DS Chertkow H The diagnosis of dementia due to Alzheimer's disease: Recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease Alzheimers Dement 2011 7 263 269 21514250 PMC3312024 source

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    • cites [22] Albert MS Dekosky ST Dickson D The diagnosis of mild cognitive impairment due to Alzheimer's disease: Recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease Alzheimers Dement 2011 7 270 279 21514249 PMC3312027 source

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  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    About half of older individuals with chronic subdural hemorrhage have cognitive deficits.

    “Subdural hemorrhage is an uncommon cause of cognitive disorder, with reports that older individuals with chronic SH have cognitive deficits in about one in two cases,61”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [61] Starkstein SE Jorge R Capizzano AA Uncommon causes of cerebrovascular dementia Int Psychogeriatr 2005 17 S51 S64 16240483 source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Hypertension, diabetes, high cholesterol, and high homocysteine have been independently linked to increased risk of Alzheimer's disease, although the evidence is inconsistent.

    “Risk factors such as hypertension, diabetes, high cholesterol and high homocysteine have been independently linked to an increased risk of Alzheimer’s disease although the evidence remains inconsistent.74–76”
    Quote in the paperNot a substantial claim0 of 3 sources checked
    • cites [74] de la Torre JC Is Alzheimer’s disease a neurodegenerative or a vascular disorder? Data, dogma, and dialectics Lancet Neurol 2004 3 184 190 14980533 source

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    • cites [75] Hendrie HC Albert MS Butters MA The NIH cognitive and emotional health project. Report of the Critical Evaluation Study Committee Alzheimer Dement 2006 2 12 32 19595852 source

      Not checked in the free run.

    • cites [76] Purnell C Gao S Callahan CM Cardiovascular risk factors and incident Alzheimer disease: a systematic review of the literature Alzheimer Dis Assoc Disord 2009 23 1 10 18703981 PMC3689425 source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Common causes of multiple hemorrhages or hemorrhagic infarcts in vascular cognitive disorder are sporadic or hereditary conditions linked to cerebral amyloid angiopathy and other genetic disorders, with hypertension possibly contributing.

    “Multiple hemorrhages or hemorrhagic infarcts are often associated with VCD, the common causes being sporadic or hereditary conditions associated with cerebral amyloid angiopathy (CAA)64 and other genetic disorders,65 although hypertension may have a role.”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [64] Attems J Jellinger K Thal DR Review: sporadic cerebral amyloid angiopathy Neuropathol Appl Neurobiol 2011 37 75 93 20946241 source

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    • cites [65] Yamamoto Y Craggs L Baumann M Molecular genetics and pathology of hereditary small vessel diseases of the brain Neuropathol Appl Neurobiol 2011 37 94 113 21062344 source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Cognitive deficits in chronic subdural hemorrhage may be progressive and are not always reversible by surgical drainage.

    “which may be progressive and not always reversible with surgical drainage.63”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [63] Ishikawa E Yanaka K Sugimoto K Reversible dementia in patients with chronic subdural hematomas J Neurosurg 2002 96 680 683 11990807 source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Other neuroimaging measures such as brain atrophy rate, hippocampal or mesial temporal atrophy, cerebral blood flow, and cerebral metabolic rate may be useful in differential diagnosis in some cases, but their status as Alzheimer's disease biomarkers is uncertain.

    “Other neuroimaging to determine the rate of brain atrophy, hippocampal or mesial temporal atrophy, cerebral blood flow and cerebral metabolic rate may be useful in the differential diagnosis in some cases, but their status as biomarkers of AD is uncertain.22”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [22] Albert MS Dekosky ST Dickson D The diagnosis of mild cognitive impairment due to Alzheimer's disease: Recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease Alzheimers Dement 2011 7 270 279 21514249 PMC3312027 source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Cerebrospinal fluid markers for Alzheimer's disease are better developed, with lower Aβ42 and elevated tau/phosphorylated-tau indicating Alzheimer's pathology.

    “CSF markers for AD are, however, better developed, with lower levels of Aβ42 and elevated levels of tau/phosphorylated-tau being indicative of AD pathology.21,22”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [21] McKhann GM Knopman DS Chertkow H The diagnosis of dementia due to Alzheimer's disease: Recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease Alzheimers Dement 2011 7 263 269 21514250 PMC3312024 source

      Not checked in the free run.

    • cites [22] Albert MS Dekosky ST Dickson D The diagnosis of mild cognitive impairment due to Alzheimer's disease: Recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease Alzheimers Dement 2011 7 270 279 21514249 PMC3312027 source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Carotid intimal-medial thickness and arterial stiffness are associated with arterial ageing and may serve as risk markers of vascular cognitive disorder.

    “Emerging markers include carotid intimal-medial thickness and arterial stiffness, which are associated with arterial ageing and may serve as risk markers of VCD.24”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [24] Gorelick PB Scuteri A Black SE Vascular contributions to cognitive impairment and dementia: a statement for healthcare professionals from the American Heart Association/American Stroke Association Stroke 2011 42 2672 2713 21778438 PMC3778669 source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Post-mortem examinations of older people with cognitive disorders usually show mixed pathologies, with vascular and Alzheimer-type pathology predominating, and other etiologies such as Lewy body disease also present.

    “Post-mortem examinations of the brains of older people who had cognitive disorders in life usually reveal a combination of pathologies with vascular lesions and Alzheimer-type pathology predominating, but stigmata of other etiologies, such as Lewy body disease, are also present.80”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [80] Neuropathology Group of the Medical Research Council Cognitive Function, and Aging Study (MRC CFAS) Pathological correlates of late-onset dementia in a multicentre, community-based population in England and Wales Lancet 2001 357 169 175 11213093

      Not checked in the free run.

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  • The paper relies on this without support.

    The term dementia has increasingly become equated with AD in the popular mind.

    “The term dementia has increasingly become equated with AD in the popular mind, even though AD accounts just over one-half of all cases of dementia.11”

  • The paper relies on this without support.

    Potentially disease-modifying treatments may be more effective before the late stage identified by the VaD threshold.

    “Yet potentially disease-modifying treatments may be more effective before this stage is reached.”

  • The paper relies on this without support.

    The temporal relationship between cerebrovascular events and cognitive impairment is not difficult to establish clinically.

    “This pattern is temporally related to cerebrovascular events of infarction, hemorrhage or vasculitis, and the temporal relationship is not difficult to establish clinically.”

  • The paper relies on this without support.

    VCD with gradual onset and slow progression is generally due to small vessel disease leading to lesions in the white matter, basal ganglia, and/or thalamus.

    “VCD with a gradual onset and slow progression is generally due to small vessel disease leading to lesions in the white matter, basal ganglia and/or thalamus.”

  • The paper relies on this without support.

    Neuropsychiatric features are not specific to vascular etiology.

    “As these neuropsychiatric features are not specific to vascular etiology, they are not considered to be core diagnostic features, yet may be the presenting symptoms.”

  • The paper relies on this without support.

    No neuroimaging feature is pathognomonic of VCD.

    “The findings are varied and there is no feature that is pathognomonic of VCD.”

  • The paper relies on this without support.

    VCD can occur without evidence of brain infarcts.

    “It is generally accepted that VCD can occur without evidence of brain infarcts, although the latter are usually present.”

  • The paper relies on this without support.

    Focal WMLs visible only on T2-weighted MRI are unlikely to be significant enough to explain the development of a cognitive disorder.

    “If the WMLs are focal and visible only on T2-weighted MRI, they are unlikely to be significant enough to explain the development of a cognitive disorder.”

  • The paper relies on this without support.

    Subdural hemorrhage is usually caused by trauma and not by vascular pathology.

    “Since SH is usually a result of trauma and not vascular pathology, it should be not be regarded as a VCD.”

  • The paper relies on this without support.

    Subarachnoid hemorrhage is due to vascular pathology.

    “SAH is due to vascular pathology and its associated cognitive deficits are appropriately regarded as VCD.”

  • The paper relies on this without support.

    Incidental brain infarctions and white matter lesions are common in the brains of older individuals.

    “Since incidental brain infarctions and WMLs are common in brains of older individuals, it is important to consider other possible etiologies when a cognitive disorder is present.”

  • The paper relies on this without support.

    Microbleeds are not uncommon in cognitively normal older individuals.

    “Since microbleeds are not uncommon in cognitively normal older individuals, attribution of the VCD to these, especially VaD, should follow a careful exclusion of other causes of cognitive impairment and only if numerous such lesions are present.”

  • The paper relies on this without support.

    Vascular cognitive disorder is often associated with psychiatric or behavioral symptoms.

    “VCD is often associated with psychiatric or behavioral symptoms that may pose special challenges for their treatment.”

  • The paper relies on this without support.

    No single profile of depression or psychosis is specific to vascular cognitive disorder.

    “While some attempts have been made to develop specific criteria for syndromes such as depression and psychosis associated with cognitive disorders,84 there is no one profile that is specific to VCD.”

  • The paper relies on this without support.

    The heterogeneity of vascular cognitive disorder has made development of reliable non-imaging biomarkers extremely challenging.

    “The heterogeneity of VCD has made the development of reliable non-imaging biomarkers extremely challenging.”

  • The paper relies on this without support.

    None of the suggested cerebrospinal fluid biomarkers is specific to vascular cognitive disorder.

    “As none of these is specific to VCD, they are not currently recommended for use for this diagnostic purpose.”
16 of 16

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Research works printed but not linked: 1

  1. Skoog, 2000, Vascular aspects in Alzheimers disease., J Neural Transm Suppl, 59, 37

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Authors
Sachdev, P., Kalaria, R., O’Brien, J., Skoog, I., Alladi, S., Black, S. E., Blacker, D., Blazer, D. G., Chen, C., Chui, H., Ganguli, M., Jellinger, K., Jeste, D. V., Pasquier, F., Paulsen, J., Prins, N., Rockwood, K., Roman, G., & Scheltens, P.
Affiliations
  • University of Southern California (US)
  • Newcastle University (GB)
  • University of Gothenburg (SE)
  • Nizam's Institute of Medical Sciences (IN)
  • Sunnybrook Health Science Centre (CA)
  • UNSW Sydney (AU)
  • Prince of Wales Hospital (AU)
  • University of Cambridge (GB)
Corresponding author
  • Sachdev, Perminder
  • Blacker, Deborah
  • Pasquier, Florence
ORCID
Venue
Alzheimer Disease & Associated Disorders
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2014-07
Volume
28
Issue
3
Pages
206-218
ISSN
0893-0341 (ISSN-L)
DOI
10.1097/wad.0000000000000034
PMC
PMC4139434
OpenAlex
W2035892177
Cited by
852
References
88
Citations by year
2026: 94 · 2025: 106 · 2024: 97 · 2023: 75 · 2022: 72 · 2021: 98 · 2020: 75 · 2019: 81 · 2018: 43 · 2017: 46 · 2016: 35 · 2015: 22 · 2014: 7 · 2013: 1
FWCI
27.97
Type
journal article
Language
en
Open access
Locations
  • Alzheimer Disease & Associated Disorders (publishedVersion)
  • PubMed (publishedVersion)
  • Pure Amsterdam UMC (publishedVersion)
  • Amsterdam UMC (VU Amsterdam) - Institutional Repository (publishedVersion)
  • PubMed Central (acceptedVersion)
  • UNSWorks (UNSW Sydney) (submittedVersion, cc-by-nc-nd)
  • eScholarship (California Digital Library) (submittedVersion)
  • UNSWorks (University of New South Wales, Sydney, Australia) (submittedVersion, cc-by-nc-nd)
  • Data Archiving and Networked Services (DANS) (submittedVersion)
  • Newcastle University ePrints (Newcastle Univesity)
Funders
  • Coordenação de Aperfeiçoamento de Pessoal de Nível Superior
  • Medical Research Council (MR/L016451/1)
  • Australian Research Council (DP120102078)
  • NIHR Newcastle Biomedical Research Centre (BH111030)
  • National Institute on Aging (P50AG005142, P50AG005134, K07AG044395, P30AG062421)
  • National Institute of Mental Health (R01MH071536)
Topics
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
  • Social Sciences › Psychology › Clinical Psychology › Historical and Modern Theater Studies
Keywords
vascular dementia, diagnostic criteria, vascular etiology, Alzheimer disease pathology, DSM-5
MeSH terms
Cognition Disorders, Humans, Dementia, Vascular

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