Skip to content

Vascular dementia — overview

TL;DR — Vascular dementia is major cognitive disorder attributable to cerebrovascular disease, but the clinically useful spectrum is vascular cognitive impairment (VCI), which includes mild and major syndromes and commonly coexists with Alzheimer pathology (Sachdev 2014, PMID 24632990; Gorelick 2011, PMID 21778438). Diagnostic confidence depends on a cognitive syndrome, objective vascular brain injury, and a defensible temporal or anatomical link between them; no single lesion count or blood marker is diagnostic (Skrobot 2018, PMID 29055812; Duering 2023, PMID 37236211). Cerebral small-vessel disease, overt stroke, cerebral amyloid angiopathy, and rare inherited arteriopathies are distinct routes to the phenotype (O'Brien 2015, PMID 26595643; Chabriat 2009, PMID 19539236). Prevention through vascular-risk control has stronger evidence than symptomatic drug treatment, and that gap widened in 2025: pooled blood-pressure trials show small reductions in dementia or cognitive impairment, a cluster-randomized trial achieving a 22 mm Hg systolic contrast in 33,995 adults reduced all-cause dementia by 15%, whereas cholinesterase inhibitors change cognitive scales by roughly 1–2 points with uncertain clinical importance (Hughes 2020, PMID 32427305; He 2025, PMID 40258956; Battle 2021, PMID 33704781). Mixed pathology is the common biological setting, so this condition is curated beside—not cleanly apart from—Alzheimer's disease (Schneider 2007, PMID 17568013).

What the label covers

Term Practical meaning Boundary problem
Vascular cognitive impairment (VCI) Umbrella from subjective or mild impairment to dementia associated with vascular brain injury Association is easier to show than causation (Gorelick 2011, PMID 21778438)
Mild vascular cognitive disorder Objective decline without loss of independence Thresholds and premorbid estimates vary (Sachdev 2014, PMID 24632990)
Major vascular cognitive disorder / vascular dementia Cognitive decline interferes with independence and is attributed predominantly to cerebrovascular disease Alzheimer and Lewy-body copathology are often occult (Schneider 2007, PMID 17568013)
Post-stroke cognitive disorder Cognitive impairment temporally related to clinical stroke Pre-stroke impairment and recurrent stroke alter denominators (Pendlebury 2009, PMID 19782001)
Subcortical ischaemic vascular disease Lacunes and white-matter injury with executive/processing-speed dysfunction Imaging burden and symptoms are not one-to-one (Duering 2023, PMID 37236211)
Mixed dementia More than one pathology materially contributes Relative contribution cannot usually be quantified clinically (Jellinger 2007, PMID 17324442)

VASCOG formalized mild and major vascular cognitive disorders and allowed memory impairment to be absent, correcting criteria that had inherited an Alzheimer-shaped requirement (Sachdev 2014, PMID 24632990). VICCCS used an international Delphi process to reduce incompatible research definitions and endorsed harmonized cognitive and imaging approaches (Skrobot 2018, PMID 29055812). The 2025 VasCog-2-WSO criteria update indicates that nosology remains active rather than settled (Sachdev 2025, PMID 40955506).

Why causal attribution is difficult

Three propositions can all be true in one person:

  1. MRI shows vascular lesions.
  2. Alzheimer biomarkers or neuropathology are present.
  3. Cognition reflects additive or interacting injury rather than a single cause.

Community autopsy data found Alzheimer pathology plus infarcts in 38.0% of people with dementia, compared with 30.0% with Alzheimer pathology alone and 12% classified as vascular dementia alone (Schneider 2007, PMID 17568013). Clinic populations differ from community autopsy cohorts, but the result defeats a simple binary taxonomy. Neuropathology reviews likewise emphasize heterogeneous infarcts, arteriolosclerosis, haemorrhages, and copathologies rather than a unitary lesion (Jellinger 2002, PMID 12417375; Jellinger 2008, PMID 18525132).

The appropriate question is therefore often “how much vascular injury is plausibly contributing?” rather than “vascular or Alzheimer?” See mixed pathology and Alzheimer overlap.

Principal substrates

Substrate Typical evidence Cognitive route Key page
Large or multiple infarcts Clinical stroke plus territorial lesions Tissue loss, disconnection, recurrent injury subtypes
Strategic infarct Thalamus, angular gyrus, basal forebrain, hippocampal or network-hub lesion Disproportionate network disruption subtypes
Sporadic small-vessel disease WMH, lacunes, microbleeds, enlarged perivascular spaces Disconnection, hypoperfusion, BBB injury small-vessel disease
Cerebral amyloid angiopathy Strictly lobar haemorrhagic lesions, cortical superficial siderosis, selected white-matter patterns Haemorrhage, microinfarction, network injury CAA
Monogenic arteriopathy Pathogenic variant plus characteristic phenotype Early, relatively tractable vascular injury inherited forms
Systemic hypoperfusion Cardiac arrest, severe hypotension, critical stenosis Watershed injury and selective vulnerability pathophysiology

STRIVE-2 standardizes visible lesions and emerging quantitative markers, but explicitly warns that small-vessel disease frequently accompanies neurodegeneration (Duering 2023, PMID 37236211). The visible MRI is a sample of cumulative injury, not a complete map of endothelial dysfunction, microinfarcts, or blood–brain barrier leakage (Wardlaw 2013, PMID 23867200).

Clinical pattern

The canonical phenotype emphasizes slowed processing, impaired set shifting, attention, and executive control with relatively less prominent encoding failure (Desmond 2004, PMID 15537510). It is a group-level tendency, not a bedside discriminator: strategic infarcts can cause focal amnesia, mixed pathology can produce an amnestic syndrome, and severe disease becomes multidomain (O'Brien 2015, PMID 26595643).

Domain Common finding Important qualifier
Processing speed Slowed timed performance Motor impairment and depression confound timed tests
Executive function Reduced flexibility, initiation, planning Not specific to vascular disease (Desmond 2004, PMID 15537510)
Memory Retrieval may exceed encoding deficit Hippocampal injury or Alzheimer copathology changes the profile
Gait Short steps, instability, dual-task cost Often tracks subcortical burden but is nonspecific
Mood/behavior Apathy, depression, emotional lability May reflect lesion location, disability, or comorbidity
Course Stepwise, fluctuating, or gradual Gradual progression is common in small-vessel disease

MoCA generally samples executive function more broadly than MMSE; a systematic review of 15 studies and 4,575 participants found heterogeneous but usually high diagnostic accuracy, insufficient for a universal cutoff (Ghafar 2019, PMID 31050033). Screening is not diagnosis and must be followed by functional history, neurological examination, laboratory evaluation, and structural imaging (Swartz 2025, PMID 39822128).

Burden and trajectory

All-dementia global estimates project growth from 57.4 million people in 2019 to 152.8 million in 2050, driven mainly by population aging and growth; this is not a vascular-dementia-specific prevalence estimate (GBD 2019 Dementia Forecasting Collaborators 2022, PMID 34998485). Vascular shares vary sharply with criteria, imaging availability, case setting, and whether mixed disease receives one label or several (Pendlebury 2009, PMID 19782001; Sachdev 2014, PMID 24632990).

After stroke, pooled estimates are more interpretable when denominators are explicit. Pendlebury and Rothwell found about 10% had dementia before a first stroke, 10% developed new dementia soon afterward, and more than one-third had dementia after recurrent stroke (Pendlebury 2009, PMID 19782001). A later hospital-based synthesis estimated any post-stroke neurocognitive disorder at 53.4% (95% CI 46.9–59.8), mild disorder at 36.4%, and major disorder at 16.5%, with thresholds and case mix explaining substantial variation (Barbay 2018, PMID 30504699).

Community incidence of vascular dementia specifically is far lower and more stable across cohorts than prevalence figures suggest: 1.5 per 1,000 person-years in the Rotterdam Study and 1.4 per 1,000 person-years (95% CI 0.6–2.3) in NEDICES, against all-dementia rates of 10.7 and 10.6 respectively (Ott 1998, PMID 9521184; Bermejo-Pareja 2008, PMID 17727890). Survival is shorter than in Alzheimer disease — non-Alzheimer dementias carry HR 1.33 (95% CI 1.21–1.46) for all-cause mortality, and vascular dementia specifically shows 1.27 fewer years (95% CI 0.65–1.90) of survival from disease onset (Liang 2021, PMID 36097997). See epidemiology and burden.

Prevention and treatment in one table

Intervention Best-supported inference Quantitative anchor
Blood-pressure treatment Small population-level reduction in cognitive outcomes; optimal target varies by frailty and symptoms OR 0.93 (95% CI 0.88–0.98) for dementia/cognitive impairment across 12 trials/92,135 participants (Hughes 2020, PMID 32427305)
Intensive BP with a large achieved contrast The one adequately powered randomized dementia-prevention success RR 0.85 (95% CI 0.76–0.95) for all-cause dementia on a 22.0 mm Hg systolic contrast over 48 months in 33,995 adults (He 2025, PMID 40258956)
Aerobic exercise in subcortical VCI Cognitive effect at least as large as any drug, not sustained after stopping ADAS-Cog −1.71 (95% CI −3.15 to −0.26) at 6 months; −0.63 (−2.34 to 1.07) six months after cessation (Liu-Ambrose 2016, PMID 27760869)
Lipid lowering Removed from the list of plausible dementia-prevention levers OR 0.96 (95% CI 0.74–1.26) across 15 trials/139,169 participants (Reddin 2025, PMID 40794911)
Intensive BP target Reduced MCI in SPRINT MIND; probable dementia endpoint nonsignificant dementia HR 0.83 (0.67–1.04); MCI HR 0.81 (0.69–0.95) (Williamson 2019, PMID 30688979)
Multidomain lifestyle Small cognitive-score benefit in selected at-risk older adults; not VaD treatment annual NTB difference 0.022 (0.002–0.042) in FINGER (Ngandu 2015, PMID 25771249)
Donepezil 5 mg Slight cognitive change, probably below clinical importance ADAS-Cog MD −0.92 (−1.44 to −0.40) (Battle 2021, PMID 33704781)
Donepezil 10 mg Larger scale change with more adverse events MD −2.21 (−3.07 to −1.35); adverse-event OR 1.95 (1.20–3.15) (Battle 2021, PMID 33704781)
Galantamine Slight cognitive change, no consistent functional benefit MD −2.01 (−3.18 to −0.85); adverse-event OR 1.57 (1.02–2.43) (Battle 2021, PMID 33704781)
Rivastigmine Uncertain benefit MD 0.03 (−3.04 to 3.10) (Battle 2021, PMID 33704781)

Risk-factor treatment is indicated for vascular outcomes on its own merits; evidence should not be inflated into proof that a specific intervention treats established vascular dementia. Conversely, small mean drug effects do not establish no individual benefit, but they require explicit discussion of adverse events and goals (Battle 2021, PMID 33704781).

Thirteen live controversies, and where each is argued

This knowledge base treats unresolved contradictions as content. The table below is the index to them; each row names two positions with citations on both sides and points to the page where the argument is developed.

# The question Position A Position B Page
1 How large are cholinesterase-inhibitor effects in VCI? raw-scale pooling gives MD −0.92 ADAS-Cog points for donepezil 5 mg (Battle 2021, PMID 33704781) standardized network meta-analysis gives SMD −1.11 for the same comparison — a "large" effect (Shi 2022, PMID 35048806) treatment
2 Do any drugs work in vascular dementia? Western reviews find nothing recommendable across 16 placebo-controlled trials (Cheng 2026, PMID 42635820) a 194-RCT Bayesian network including Chinese-language literature ranks butylphthalide and huperzine A highest (Dang 2024, PMID 39239652) treatment
3 Does blood-pressure lowering prevent dementia? Largely resolved in 2025: a cluster-randomized trial in 33,995 rural Chinese adults achieved a 22.0 mm Hg systolic contrast over 48 months and reduced all-cause dementia, RR 0.85 (95% CI 0.76–0.95) — consistent with the older Syst-Eur signal (He 2025, PMID 40258956; Forette 1998, PMID 9802273; Forette 2002, PMID 12374512) The placebo-controlled literature at small contrasts remains null: Cochrane OR 0.89 (0.72–1.09), very low certainty, and no trial has yet shown an effect on adjudicated vascular dementia (Cunningham 2021, PMID 34028812) prevention
4 Is WMH causal for dementia? two-sample Mendelian randomization: OR 1.43 (1.10–1.86) for Alzheimer disease individual-level longitudinal analysis in the same paper: HR 1.02 (1.00–1.04), null (Sargurupremraj 2024, PMID 38776079) small-vessel disease
5 Should imaging or cognition define benefit? intensive BP reduces global SVD burden with a dose-response (Cohen's d −0.40) (Charisis 2026, PMID 42614618) ESO–EAN concludes cognitive benefit of vascular risk treatment after stroke is not proven (Quinn 2021, PMID 34746430) guidelines
6 Is EGb 761 a legitimate option? Asian expert consensus grades it at cholinesterase-inhibitor strength, Level B (Kandiah 2019, PMID 30648358) Cochrane finds 6-month benefit with I² 91–96% and low certainty; European guidance does not recommend it (Wieland 2026, PMID 41641880; Quinn 2021, PMID 34746430) guidelines
7 Is "cerebrovascular disease" one exposure? criteria and cohorts code it as present/absent single CVD pathologies do not accelerate decline; only mixtures do (Lamar 2022, PMID 34601898) mixed pathology
8 Is CADASIL rare? clinical prevalence ~2–5 per 100,000 adults (Razvi 2005, PMID 15834040; Moreton 2014, PMID 24840674) genetic prevalence 1 in 277 in 129,933 sequenced adults (Cho 2025, PMID 40982447) inherited forms

| 9 | Do perivascular spaces carry cognitive information? | severe PVS in both regions predicts incident dementia, OR 2.91 (1.43–5.95) over 8 years (Paradise 2021, PMID 33504642) | no cross-sectional cognitive association across five harmonized cohorts (n=3,575), and PVS volume predicts nothing in established SVD (Hilal 2018, PMID 30068634; Hong 2024, PMID 38465597) | small-vessel disease | | 10 | Is vascular dementia the agitated or the apathetic dementia? | long-term-care registry (n=10,405): lower agitation, higher apathy than Alzheimer disease (Schwertner 2022, PMID 35491774) | memory-clinic series (n=180): more agitation (40% vs 14%) and sleep disturbance (Anor 2017, PMID 28245482) | patient experience | | 11 | Is caregiving harder in vascular or Alzheimer dementia? | Alzheimer caregivers report higher burden on every CBI subscale in 506 clinic patients (D'Onofrio 2015, PMID 25475248) | stratified by severity, vascular dementia imposes the greater burden at mild-to-moderate stages and the relationship reverses only in severe disease (Vetter 1999, PMID 10097779) | patient experience | | 12 | Does CAA cause dementia independently of Alzheimer pathology? | ACT autopsy cohort: association disappears after adjustment for Braak stage (OR 0.96, 0.69–1.33), 111% mediated (Sin 2024, PMID 39481068) | HAAS autopsy cohort: CASI 45.9% lower in Alzheimer-plus-CAA versus 16.6% in Alzheimer alone — a conditional effect that mediation framing hides (Pfeifer 2002, PMID 12058090) | CAA | | 13 | Do vascular criteria have low autopsy sensitivity? | hospital autopsy series: probable-tier sensitivity 0.20–0.25 (Gold 2002, PMID 11772694) | population-based series using disjunctive criteria: sensitivity 0.75, specificity 0.81, LR+ 3.9 (2.2–6.7) (Knopman 2003, PMID 12707071) | nosology |

A fourteenth tension runs beneath several of these: the diagnostic criteria that define trial populations have autopsy sensitivities of 0.20–0.25 at the "probable" tier (Gold 2002, PMID 11772694), so the population in which drug effects are measured may not be the population the label describes — see nosology.

Research and measurement priorities

  • Standardize causal attribution without pretending that mixed pathology disappears (Sachdev 2025, PMID 40955506).
  • Validate imaging and fluid markers against longitudinal cognition and neuropathology (Duering 2023, PMID 37236211).
  • Build trials around mechanistically coherent phenotypes rather than broad “probable VaD” labels (Markus 2022, PMID 35969390).
  • Separate prevention of stroke, prevention of cognitive decline, and symptomatic cognitive benefit as different endpoints (Peters 2022, PMID 36282295).
  • Include function, caregiver outcomes, and participation alongside cognitive scales (Swartz 2025, PMID 39822128).

Open questions

  • Can VasCog-2-WSO improve inter-rater reliability and trial enrichment without excluding mixed disease? (Sachdev 2025, PMID 40955506)
  • Which quantitative small-vessel markers add prediction beyond age, stroke burden, WMH, and baseline cognition? (Duering 2023, PMID 37236211)
  • Does preventing recurrent stroke proportionally prevent delayed dementia, and in which etiologic subgroups? (Filler 2024, PMID 38101426)
  • What minimum cognitive and functional effect would make cholinesterase inhibition worthwhile to patients? (Battle 2021, PMID 33704781)

References

  1. Sachdev PS, et al. Diagnostic criteria for vascular cognitive disorders: a VASCOG statement. Alzheimer Dis Assoc Disord. 2014. PMID 24632990
  2. Skrobot OA, et al. Progress toward standardized diagnosis of vascular cognitive impairment. Alzheimers Dement. 2018. PMID 29055812
  3. VasCog-2-WSO Criteria Consortium. Revised Diagnostic Criteria for Vascular Cognitive Impairment and Dementia—The VasCog-2-WSO Criteria. JAMA Neurol. 2025. PMID 40955506
  4. Gorelick PB, et al. Vascular contributions to cognitive impairment and dementia. Stroke. 2011. PMID 21778438
  5. O'Brien JT, Thomas A. Vascular dementia. Lancet. 2015. PMID 26595643
  6. Duering M, et al. Neuroimaging standards for research into small vessel disease—advances since 2013. Lancet Neurol. 2023. PMID 37236211
  7. Wardlaw JM, et al. Neuroimaging standards for research into small vessel disease and its contribution to ageing and neurodegeneration. Lancet Neurol. 2013. PMID 23867200
  8. Schneider JA, et al. Mixed brain pathologies account for most dementia cases in community-dwelling older persons. Neurology. 2007. PMID 17568013
  9. Jellinger KA. The pathology of ischemic-vascular dementia: an update. J Neurol Sci. 2002. PMID 12417375
  10. Jellinger KA, Attems J. Neuropathological evaluation of mixed dementia. J Neurol Sci. 2007. PMID 17324442
  11. Jellinger KA. The pathology of vascular dementia: a critical update. J Alzheimers Dis. 2008. PMID 18525132
  12. Desmond DW. The neuropsychology of vascular cognitive impairment. J Neurol Sci. 2004. PMID 15537510
  13. Ghafar MZAA, et al. Cognitive screening instruments to identify vascular cognitive impairment: a systematic review. Int J Geriatr Psychiatry. 2019. PMID 31050033
  14. Swartz RH, et al. Canadian Stroke Best Practice Recommendations: Vascular cognitive impairment, 7th edition update, 2024. Alzheimers Dement. 2025. PMID 39822128
  15. Pendlebury ST, Rothwell PM. Prevalence, incidence, and factors associated with pre-stroke and post-stroke dementia. Lancet Neurol. 2009. PMID 19782001
  16. Barbay M, et al. Prevalence of post-stroke neurocognitive disorders in hospital-based studies. Dement Geriatr Cogn Disord. 2018. PMID 30504699
  17. GBD 2019 Dementia Forecasting Collaborators. Estimation of global dementia prevalence in 2019 and forecast to 2050. Lancet Public Health. 2022. PMID 34998485
  18. Hughes D, et al. Association of blood pressure lowering with incident dementia or cognitive impairment. JAMA. 2020. PMID 32427305
  19. Williamson JD, et al. Effect of intensive versus standard blood pressure control on probable dementia. JAMA. 2019. PMID 30688979
  20. Peters R, et al. Blood pressure lowering and prevention of dementia: individual patient data meta-analysis. Eur Heart J. 2022. PMID 36282295
  21. Ngandu T, et al. A 2-year multidomain intervention to prevent cognitive decline: FINGER. Lancet. 2015. PMID 25771249
  22. Battle CE, et al. Cholinesterase inhibitors for vascular dementia and other vascular cognitive impairments. Cochrane Database Syst Rev. 2021. PMID 33704781
  23. Filler J, et al. Risk factors for cognitive impairment and dementia after stroke. Lancet Healthy Longev. 2024. PMID 38101426
  24. Chabriat H, et al. CADASIL. Lancet Neurol. 2009. PMID 19539236
  25. Markus HS, et al. Framework for Clinical Trials in Cerebral Small Vessel Disease (FINESSE). JAMA Neurol. 2022. PMID 35969390
  26. Shi X, et al. Comparative efficacy and acceptability of cholinesterase inhibitors and memantine in vascular cognitive impairment: a network meta-analysis. Curr Alzheimer Res. 2022;19:133-145. PMID 35048806
  27. Cheng T, et al. Pharmacological interventions targeting cognition in vascular dementia: systematic review and meta-analysis. Eur J Clin Pharmacol. 2026;82:240. PMID 42635820
  28. Dang C, et al. Pharmacological treatments for vascular dementia: a Bayesian network meta-analysis. Front Pharmacol. 2024;15:1451032. PMID 39239652
  29. Forette F, et al. Prevention of dementia in the Syst-Eur trial. Lancet. 1998;352:1347-51. PMID 9802273
  30. Forette F, et al. Prevention of dementia with antihypertensive treatment: Syst-Eur extended follow-up. Arch Intern Med. 2002;162:2046-52. PMID 12374512
  31. Cunningham EL, et al. Pharmacological treatment of hypertension for the prevention of cognitive impairment and dementia. Cochrane Database Syst Rev. 2021;5:CD004034. PMID 34028812
  32. Sargurupremraj M, et al. Genetic complexities of cerebral small vessel disease, blood pressure, and dementia. JAMA Netw Open. 2024;7:e2412824. PMID 38776079
  33. Charisis S, et al. Intensive versus standard blood pressure control and overall brain small vessel disease burden: post-hoc analysis of SPRINT. EClinicalMedicine. 2026;99:104143. PMID 42614618
  34. Quinn TJ, et al. ESO–EAN joint guidelines on post-stroke cognitive impairment. Eur Stroke J. 2021;6:I-XXXVIII. PMID 34746430
  35. Kandiah N, et al. Expert consensus on the use of Ginkgo biloba extract EGb 761 in neurocognitive disorders. CNS Neurosci Ther. 2019;25:288-298. PMID 30648358
  36. Wieland LS, et al. Ginkgo biloba for cognitive impairment and dementia. Cochrane Database Syst Rev. 2026;2:CD013661. PMID 41641880
  37. Lamar M, et al. Complex profiles of cerebrovascular disease pathologies in the aging brain. Stroke. 2022;53:218-227. PMID 34601898
  38. Razvi SS, et al. The prevalence of CADASIL in the west of Scotland. J Neurol Neurosurg Psychiatry. 2005;76:739-41. PMID 15834040
  39. Moreton FC, et al. Changing clinical patterns and increasing prevalence in CADASIL. Acta Neurol Scand. 2014;130:197-203. PMID 24840674
  40. Cho EH, et al. Genetic epidemiology of moyamoya disease and CADASIL in over 120,000 healthy Korean individuals. PLoS One. 2025;20:e0331174. PMID 40982447
  41. Gold G, et al. Clinicopathological validation study of four sets of clinical criteria for vascular dementia. Am J Psychiatry. 2002;159:82-7. PMID 11772694
  42. Ott A, et al. Incidence and risk of dementia. The Rotterdam Study. Am J Epidemiol. 1998;147:574-80. PMID 9521184
  43. Bermejo-Pareja F, et al. Incidence and subtypes of dementia in three elderly populations of central Spain. J Neurol Sci. 2008;264:63-72. PMID 17727890
  44. Liang CS, et al. Mortality rates in Alzheimer's disease and non-Alzheimer's dementias: a systematic review and meta-analysis. Lancet Healthy Longev. 2021;2:e479-e488. PMID 36097997
  45. He J, et al. Blood pressure reduction and all-cause dementia in people with uncontrolled hypertension: an open-label, blinded-endpoint, cluster-randomized trial. Nat Med. 2025;31:2054-2061. PMID 40258956
  46. Liu-Ambrose T, et al. Aerobic exercise and vascular cognitive impairment: a randomized controlled trial. Neurology. 2016;87:2082-2090. PMID 27760869
  47. Reddin C, et al. Association of lipid-lowering therapy with dementia and cognitive outcomes: a systematic review and meta-analysis. Age Ageing. 2025;54:afaf219. PMID 40794911
  48. Paradise M, et al. Association of dilated perivascular spaces with cognitive decline and incident dementia. Neurology. 2021;96:e1501-e1511. PMID 33504642
  49. Hilal S, et al. Enlarged perivascular spaces and cognition: a meta-analysis of 5 population-based studies. Neurology. 2018;91:e832-e842. PMID 30068634
  50. Hong H, et al. Relationship of perivascular space markers with incident dementia in cerebral small vessel disease. Stroke. 2024;55:1032-1040. PMID 38465597
  51. Schwertner E, et al. Behavioral and psychological symptoms of dementia in different dementia disorders: a large-scale study of 10,000 individuals. J Alzheimers Dis. 2022;87:1307-1318. PMID 35491774
  52. Anor CJ, et al. Neuropsychiatric symptoms in Alzheimer disease, vascular dementia, and mixed dementia. Neurodegener Dis. 2017;17:127-134. PMID 28245482
  53. D'Onofrio G, et al. Caregiver burden characterization in patients with Alzheimer's disease or vascular dementia. Int J Geriatr Psychiatry. 2015;30:891-9. PMID 25475248
  54. Vetter PH, et al. Vascular dementia versus dementia of Alzheimer's type: do they have differential effects on caregivers' burden? J Gerontol B Psychol Sci Soc Sci. 1999;54:S93-8. PMID 10097779
  55. Sin MK, et al. Cerebral amyloid angiopathy, dementia, and Alzheimer neuropathologic changes: findings from the ACT autopsy cohort. Neurology. 2024;103:e210009. PMID 39481068
  56. Pfeifer LA, et al. Cerebral amyloid angiopathy and cognitive function: the HAAS autopsy study. Neurology. 2002;58:1629-34. PMID 12058090
  57. Knopman DS, et al. Vascular dementia in a population-based autopsy study. Arch Neurol. 2003;60:569-75. PMID 12707071