Vascular dementia

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Vascular dementia
Other namesDementia due to cerebrovascular disease; [1]
Vascular cognitive impairment [2]
BrainAtrophy(exvacuo).png
Brain atrophy from vascular dementia
Specialty Psychiatry, neurology   OOjs UI icon edit-ltr-progressive.svg
Symptoms Cognitive impairment, short-term memory loss [3]
Complications Heart disease, loss of ability to care for self and interact, pneumonia [4]
CausesConditions that impair blood vessels in the brain and therefore interfere with oxygen delivery to the brain [3]
Risk factors High blood pressure, high cholesterol, atrial fibrillation, diabetes [3]
Diagnostic method Lab test, neuroimaging test, neuropsychological testing [5]
Differential diagnosis Alzheimer’s disease [5]
Treatment Symptomatic [3] [4]
Frequency15-30% of dementia cases in the United States, Europe, and Asia [5] [6]

Vascular dementia is dementia caused by a series of strokes. [2] [4] Restricted blood flow due to strokes reduces oxygen and glucose delivery to the brain, causing cell injury and neurological deficits in the affected region. [6] Subtypes of vascular dementia include subcortical vascular dementia, multi-infarct dementia, stroke-related dementia, and mixed dementia. [2] [5]

Contents

Subcortical vascular dementia occurs from damage to small blood vessels in the brain. Multi-infarct dementia results from a series of small strokes affecting several brain regions. Stroke-related dementia involving successive small strokes causes a more gradual decline in cognition. [4] Dementia may occur when neurodegenerative and cerebrovascular pathologies are mixed, as in susceptible elderly people (75 years and older). [2] [5] Cognitive decline can be traced back to occurrence of successive strokes. [4]

ICD-11 lists vascular dementia as dementia due to cerebrovascular disease. [1] DSM-5 lists vascular dementia as either major or mild vascular neurocognitive disorder. [7]

Signs and symptoms

People with vascular dementia present with progressive cognitive impairment, acutely or sub-acutely as in mild cognitive impairment, frequently step-wise, after multiple strokes. [5]

The disease is described as both a mental and behavioral disorder within the ICD-11. [8] Signs and symptoms are cognitive, motor, behavioral, and for a significant proportion of people, also affective. These changes typically occur over a period of 5–10 years. Signs are typically the same as in other dementias, but mainly include cognitive decline and memory impairment of sufficient severity as to interfere with activities of daily living, sometimes with presence of focal neurological signs, and evidence of features consistent with cerebrovascular disease on brain imaging (CT or MRI). [4] [5]

The neurological signs localizing to certain areas of the brain that can be observed are hemiparesis, bradykinesia, hyperreflexia, extensor plantar reflexes, ataxia, pseudobulbar palsy, as well as gait problems and swallowing difficulties. People have patchy deficits in terms of cognitive testing. They tend to have better free recall and fewer recall intrusions when compared with people having Alzheimer's disease. [9] In the more severely affected people, or those affected by infarcts in Wernicke's or Broca's areas, specific problems with speaking called dysarthria and aphasias may be present. [2] [5]

In small vessel disease, the frontal lobes are often affected. Consequently, people with vascular dementia tend to perform worse than their Alzheimer's disease counterparts in frontal lobe tasks, such as verbal fluency, and may present with frontal lobe problems: apathy, abulia (lack of will or initiative), problems with attention, orientation, and urinary incontinence. They tend to exhibit more perseverative behavior. People with vascular dementia may also present with general slowing of processing ability, difficulty shifting sets, and impairment in abstract thinking. Apathy early in the disease is more suggestive of vascular dementia. [2] [5]

Rare genetic disorders that cause vascular lesions in the brain have other presentation patterns. As a rule, they tend to occur earlier in life and have a more aggressive course. In addition, infectious disorders, such as syphilis, can cause arterial damage, strokes, and bacterial inflammation of the brain. [10]

Causes

Risk factors and clinical characteristics for vascular dementia Fcvm-08-803169-g0001.jpg
Risk factors and clinical characteristics for vascular dementia

Vascular dementia can be caused by ischemic or hemorrhagic infarcts affecting multiple brain areas, including the anterior cerebral artery territory, the parietal lobes, or the cingulate gyrus. [5] On rare occasion, infarcts in the hippocampus or thalamus are the cause of dementia. [12] A history of stroke increases the risk of developing dementia by around 70%, and recent stroke increases the risk by around 120%. [13] Brain vascular lesions can also be the result of diffuse cerebrovascular disease, such as small vessel disease. [5]

Risk factors

Risk factors for vascular dementia include increasing age, hypertension, smoking, hypercholesterolemia, diabetes mellitus, cardiovascular disease, and cerebrovascular disease. [2] [5] Other risk factors include lifestyle, geographic origin, and APOE-ε4 genotype. [2] [5]

Vascular dementia can sometimes be triggered by cerebral amyloid angiopathy, which involves accumulation of amyloid beta plaques in the walls of the cerebral arteries, leading to breakdown and rupture of the vessels. [2] [5] Since amyloid plaques are a characteristic feature of Alzheimer's disease, vascular dementia may occur as a consequence. [2] [6]

Diagnosis

Several specific diagnostic criteria can be used to diagnose vascular dementia, including the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) criteria, the International Classification of Diseases, Tenth Edition (ICD-10) criteria, the National Institute of Neurological Disorders and Stroke criteria, Association Internationale pour la Recherche et l'Enseignement en Neurosciences (NINDS-AIREN) criteria, the Alzheimer's Disease Diagnostic and Treatment Center criteria, and the Hachinski Ischemic Score (after Vladimir Hachinski). [2] [6] [14]

The recommended investigations for cognitive impairment include: blood tests (for anemia, vitamin deficiency, thyrotoxicosis, infection, among others), chest xray, ECG, and neuroimaging, preferably a scan with a functional or metabolic sensitivity beyond a simple CT or MRI. [2] [4] When available as a diagnostic tool, single photon emission computed tomography (SPECT) and positron emission tomography (PET) neuroimaging may be used to confirm a diagnosis of multi-infarct dementia in conjunction with evaluations involving mental status examination. [2] [4] [6]

In a person already having dementia, SPECT appears to be superior in differentiating multi-infarct dementia from Alzheimer's disease, compared to the usual mental testing and medical history analysis. [15] [ additional citation(s) needed ]

The screening blood tests typically include full blood count, liver function tests, thyroid function tests, lipid profile, erythrocyte sedimentation rate, C reactive protein, syphilis serology, calcium serum level, fasting glucose, urea, electrolytes, vitamin B-12, and folate. [4] [6]

Differential diagnosis

Differentiating dementia syndromes can be challenging, due to the frequently overlapping clinical features and related underlying pathology. Mixed dementia, involving two types of dementia, can occur. In particular, Alzheimer's disease often co-occurs with vascular dementia. [2] [5]

Mixed dementia is diagnosed when people have evidence of Alzheimer's disease and cerebrovascular disease, either clinically or based on neuro-imaging evidence of ischemic lesions. [16]

Pathology

Gross examination of the brain may reveal noticeable lesions and damage to blood vessels. [2] [6] Accumulation of various substances such as lipid deposits and clotted blood appear on microscopic views. The white matter is substantially affected, with noticeable atrophy (tissue loss), in addition to calcification of the arteries. [2] [6] [17] Microinfarcts may also be present in the gray matter (cerebral cortex), sometimes in large numbers. [2]

Although atheroma of the major cerebral arteries is typical in vascular dementia, smaller vessels and arterioles are mainly affected. [2] [6]

Prevention

Early detection and accurate diagnosis are important, as vascular dementia is at least partially preventable. Ischemic changes in the brain are irreversible, but the person with vascular dementia can demonstrate periods of stability or even mild improvement. [18] Since stroke is an essential part of vascular dementia, [13] the goal is to prevent new strokes. This is attempted through reduction of stroke risk factors, such as high blood pressure, high blood lipid levels, atrial fibrillation, or diabetes mellitus. [2] [5]

Medications for high blood pressure are used to prevent pre-stroke dementia. [19] These medications include angiotensin converting enzyme inhibitors, diuretics, calcium channel blockers, sympathetic nerve inhibitors, angiotensin II receptor antagonists or adrenergic antagonists.[ medical citation needed ]

A 2023 review found that therapy with statin drugs was ineffective in treating or preventing stroke or dementia in people without a history of cerebrovascular disease. [20]

Treatment

As of 2024, there are no medications used specifically for prevention or treatment of vascular dementia. [4] [3]

Prognosis

Many studies have been conducted to determine average survival of people with dementia. The studies were frequently small and limited, which caused contradictory results in the connection of mortality to the type of dementia and the person's gender. One 2015 study found that the one-year mortality was three to four times higher in people after their first referral to a day clinic for dementia, when compared to the general population. [21] If the person was hospitalized for dementia, the mortality was even higher than in people hospitalized for cardiovascular disease. [21] Vascular dementia was found to have either comparable or worse survival rates when compared to Alzheimer's disease; [22] another 2014 study found that the prognosis for people with vascular dementia was worse for male and older people. [23]

Vascular dementia may be a direct cause of death due to the possibility of a fatal interruption in the brain's blood supply. [24]

Epidemiology

Vascular dementia is the second-most-common form of dementia after Alzheimer's disease in older adults. [4] The prevalence of the illness is 1.5% in Western countries and approximately 2.2% in Japan. It accounts for 50% of all dementias in Japan, 20% to 40% in Europe and 15% in Latin America. 25% of people with stroke develop new-onset dementia within one year of their stroke. One study found that in the United States, the prevalence of vascular dementia in all people over the age of 71 is 2.43%, and another found that the prevalence of the dementias doubles with every 5.1 years of age.[ citation needed ]

The incidence peaks between the fourth and the seventh decades of life and 80% of people have a history of hypertension. [25] [ additional citation(s) needed ]

A 2018 meta-analysis identified 36 studies of prevalent stroke (1.9 million participants) and 12 studies of incident stroke (1.3 million participants). [13] For prevalent stroke, the pooled hazard ratio for all-cause dementia was 1.69; for incident stroke, the pooled risk ratio was 2.18. [13] Study characteristics did not modify these associations, with the exception of sex, which explained 50.2% of between-study heterogeneity for prevalent stroke. These results confirm that stroke is a strong, independent, and potentially modifiable risk factor for all-cause dementia. [13]

See also

Related Research Articles

<span class="mw-page-title-main">Dementia</span> Long-term brain disorders causing impaired memory, thinking and behavior

Dementia is a syndrome associated with many neurodegenerative diseases, characterized by a general decline in cognitive abilities that affects a person's ability to perform everyday activities. This typically involves problems with memory, thinking, behavior, and motor control. Aside from memory impairment and a disruption in thought patterns, the most common symptoms of dementia include emotional problems, difficulties with language, and decreased motivation. The symptoms may be described as occurring in a continuum over several stages. Dementia ultimately has a significant effect on the individual, their caregivers, and their social relationships in general. A diagnosis of dementia requires the observation of a change from a person's usual mental functioning and a greater cognitive decline than might be caused by the normal aging process.

<span class="mw-page-title-main">Dementia with Lewy bodies</span> Type of progressive dementia

Dementia with Lewy bodies (DLB) is a type of dementia characterized by changes in sleep, behavior, cognition, movement, and regulation of automatic bodily functions. Memory loss is not always an early symptom. The disease worsens over time and is usually diagnosed when cognitive impairment interferes with normal daily functioning. Together with Parkinson's disease dementia, DLB is one of the two Lewy body dementias. It is a common form of dementia, but the prevalence is not known accurately and many diagnoses are missed. The disease was first described on autopsy by Kenji Kosaka in 1976, and he named the condition several years later.

<span class="mw-page-title-main">Binswanger's disease</span> Medical condition

Binswanger's disease, also known as subcortical leukoencephalopathy and subcortical arteriosclerotic encephalopathy, is a form of small-vessel vascular dementia caused by damage to the white brain matter. White matter atrophy can be caused by many circumstances including chronic hypertension as well as old age. This disease is characterized by loss of memory and intellectual function and by changes in mood. These changes encompass what are known as executive functions of the brain. It usually presents between 54 and 66 years of age, and the first symptoms are usually mental deterioration or stroke.

<span class="mw-page-title-main">Cerebrovascular disease</span> Condition that affects the arteries that supply the brain

Cerebrovascular disease includes a variety of medical conditions that affect the blood vessels of the brain and the cerebral circulation. Arteries supplying oxygen and nutrients to the brain are often damaged or deformed in these disorders. The most common presentation of cerebrovascular disease is an ischemic stroke or mini-stroke and sometimes a hemorrhagic stroke. Hypertension is the most important contributing risk factor for stroke and cerebrovascular diseases as it can change the structure of blood vessels and result in atherosclerosis. Atherosclerosis narrows blood vessels in the brain, resulting in decreased cerebral perfusion. Other risk factors that contribute to stroke include smoking and diabetes. Narrowed cerebral arteries can lead to ischemic stroke, but continually elevated blood pressure can also cause tearing of vessels, leading to a hemorrhagic stroke.

<span class="mw-page-title-main">Caudate nucleus</span> Structure of the striatum in the basal ganglia of the brain

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<span class="mw-page-title-main">Frontotemporal dementia</span> Types of dementia involving the frontal or temporal lobes

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<span class="mw-page-title-main">Primary progressive aphasia</span> Gradual impairment of language processing capabilities

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<span class="mw-page-title-main">Perivascular space</span> Space surrounding blood vessels

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Memory disorders are the result of damage to neuroanatomical structures that hinders the storage, retention and recollection of memories. Memory disorders can be progressive, including Alzheimer's disease, or they can be immediate including disorders resulting from head injury.

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Mild cognitive impairment (MCI) is a neurocognitive disorder which involves cognitive impairments beyond those expected based on an individual's age and education but which are not significant enough to interfere with instrumental activities of daily living. MCI may occur as a transitional stage between normal aging and dementia, especially Alzheimer's disease. It includes both memory and non-memory impairments. The cause of the disorder remains unclear, as well as both its prevention and treatment, with some 50 percent of people diagnosed with it going on to develop Alzheimer's disease within five years. The diagnosis can also serve as an early indicator for other types of dementia, although MCI may remain stable or even remit.

The prevention of dementia involves reducing the number of risk factors for the development of dementia, and is a global health priority needing a global response. Initiatives include the establishment of the International Research Network on Dementia Prevention (IRNDP) which aims to link researchers in this field globally, and the establishment of the Global Dementia Observatory a web-based data knowledge and exchange platform, which will collate and disseminate key dementia data from members states. Although there is no cure for dementia, it is well established that modifiable risk factors influence both the likelihood of developing dementia and the age at which it is developed. Dementia can be prevented by reducing the risk factors for vascular disease such as diabetes, high blood pressure, obesity, smoking, physical inactivity and depression. A study concluded that more than a third of dementia cases are theoretically preventable. Among older adults both an unfavorable lifestyle and high genetic risk are independently associated with higher dementia risk. A favorable lifestyle is associated with a lower dementia risk, regardless of genetic risk. In 2020, a study identified 12 modifiable lifestyle factors, and the early treatment of acquired hearing loss was estimated as the most significant of these factors, potentially preventing up to 9% of dementia cases.

<span class="mw-page-title-main">Leukoaraiosis</span> Type of white matter abnormality near the lateral ventricles

Leukoaraiosis is a particular abnormal change in appearance of white matter near the lateral ventricles. It is often seen in aged individuals, but sometimes in young adults. On MRI, leukoaraiosis changes appear as white matter hyperintensities (WMHs) in T2 FLAIR images. On CT scans, leukoaraiosis appears as hypodense periventricular white-matter lesions.

<span class="mw-page-title-main">Alzheimer's disease</span> Progressive neurodegenerative disease

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<span class="mw-page-title-main">Hyperintensity</span> High intensity on MRI brain scans

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<span class="mw-page-title-main">Vladimir Hachinski</span> Canadian clinical neuroscientist

Vladimir Hachinski is a Canadian clinical neuroscientist and researcher based at the Schulich School of Medicine and Dentistry at Western University. He is also a Senior Scientist at London's Robarts Research Institute. His research pertains in the greatest part to stroke and dementia, the interactions between them and their joint prevention through holistic brain health promotion. He and John W. Norris helped to establish the world's first successful stroke unit at Sunnybrook Hospital in Toronto, and, by extension, helped cement stroke units as the standard of care for stroke patients everywhere. He discovered that the control of the heart by the brain is asymmetric, the fight/flight (sympathetic) response being controlled by the right hemisphere and the rest and digest (parasympathetic) response being controlled by the left hemisphere and damage to one key component can lead to heart irregularities and sudden death. This discovery has added fundamental knowledge to how the brain controls the heart and blood pressure and lays the foundation for helping prevent sudden death.

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<span class="mw-page-title-main">Hypertension and the brain</span>

Hypertension is a condition characterized by an elevated blood pressure in which the long term consequences include cardiovascular disease, kidney disease, adrenal gland tumors, vision impairment, memory loss, metabolic syndrome, stroke and dementia. It affects nearly 1 in 2 Americans and remains as a contributing cause of death in the United States. There are many genetic and environmental factors involved with the development of hypertension including genetics, diet, and stress.

References

  1. 1 2 "ICD-11: Dementia due to cerebrovascular disease". World Health Organization. 2024. Retrieved 10 April 2024.
  2. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 Iadecola C, Duering M, Hachinski V, Joutel A, Pendlebury ST, Schneider JA, et al. (July 2019). "Vascular Cognitive Impairment and Dementia". Journal of the American College of Cardiology. 73 (25): 3326–3344. doi:10.1016/j.jacc.2019.04.034. PMC   6719789 . PMID   31248555.
  3. 1 2 3 4 5 "Vascular dementia". National Heart, Lung, and Blood Institute, US National Institutes of Health. 28 September 2022. Retrieved 10 April 2024.
  4. 1 2 3 4 5 6 7 8 9 10 11 "Vascular dementia". MedlinePlus, US National Library of Medicine.
  5. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 Sanders AE, Schoo C, Kalish VB (22 October 2023). "Vascular dementia". StatPearls, US National Library of Medicine. PMID   28613567 . Retrieved 9 April 2024.
  6. 1 2 3 4 5 6 7 8 9 Wong CE, Chui CH (June 2022). "Vascular cognitive impairment and dementia". Continuum. 28 (3): 750–780. doi:10.1212/CON.0000000000001124. PMC   9833847 . PMID   35678401.
  7. ↑ American Psychiatric Association (2013). Diagnostic and statistical manual of mental disorders : DSM-5 (5th ed.). Washington, DC: American Psychiatric Association. pp.  591–603. ISBN   978-0-89042-554-1.
  8. ↑ "ICD-11 for Mortality and Morbidity Statistics". icd.who.int. Retrieved 2022-12-09.
  9. ↑ Alagiakrishnan K. "Vascular Dementia Clinical Presentation: History, Physical, Causes". emedicine.medscape.com. Retrieved 2021-03-19.
  10. ↑ Cannistraro RJ, Badi M, Eidelman BH, Dickson DW, Middlebrooks EH, Meschia JF (2019-06-11). "CNS small vessel disease: A clinical review". Neurology. 92 (24): 1146–1156. doi:10.1212/WNL.0000000000007654. ISSN   1526-632X. PMC   6598791 . PMID   31142635.
  11. ↑ Mossanen Parsi M, Duval C, Ariëns R (2021). "Vascular dementia and crosstalk between the complement and coagulation systems". Frontiers in Cardiovascular Medicine. 8: 803169. doi: 10.3389/fcvm.2021.803169 . PMC   8733168 . PMID   35004913.
  12. ↑ Kaur M, Sharma S (1 February 2022). "Molecular mechanisms of cognitive impairment associated with stroke". Metabolic Brain Disease. 37 (2): 279–287. doi:10.1007/s11011-022-00901-0. ISSN   1573-7365. PMID   35029798.
  13. 1 2 3 4 5 Kuźma E, Lourida I, Moore SF, Levine DA, Ukoumunne OC, Llewellyn DJ (November 2018). "Stroke and dementia risk: A systematic review and meta-analysis". Alzheimer's & Dementia. 14 (11): 1416–1426. doi:10.1016/j.jalz.2018.06.3061. PMC   6231970 . PMID   30177276.
  14. ↑ Robinson L, Tang E, Taylor JP (16 June 2015). "Dementia: timely diagnosis and early intervention". BMJ. 350: h3029. doi:10.1136/bmj.h3029. ISSN   1756-1833. PMC   4468575 . PMID   26079686.
  15. ↑ Engelhardt E, Tocquer C, André C, Moreira DM, Okamoto IH, Cavalcanti J, et al. (October 2011). "Vascular dementia: Diagnostic criteria and supplementary exams. Recommendations of the Scientific Department of Cognitive Neurology and Aging of the Brazilian Academy of Neurology. Part I." Dementia & Neuropsychologia. 5 (4): 251–263. doi:10.1590/S1980-57642011DN05040003. PMC   5619038 . PMID   29213752.
  16. ↑ Custodio N, Montesinos R, Lira D, Herrera-Pérez E, Bardales Y, Valeriano-Lorenzo L (2017). "Mixed dementia: A review of the evidence". Dementia & Neuropsychologia. 11 (4): 364–370. doi:10.1590/1980-57642016dn11-040005. ISSN   1980-5764. PMC   5769994 . PMID   29354216.
  17. ↑ Hase Y, Horsburgh K, Ihara M, Kalaria RN (2018). "White matter degeneration in vascular and other ageing-related dementias". Journal of Neurochemistry. 144 (5): 617–633. doi: 10.1111/jnc.14271 . hdl: 20.500.11820/780992bd-e933-4715-8099-c4d463070a58 . PMID   29210074. S2CID   33778577.
  18. ↑ Erkinjuntti T (February 2012). Gelder M, Andreasen N, Lopez-Ibor J, Geddes J (eds.). New Oxford Textbook of Psychiatry (2 ed.). Oxford: Oxford University Press. doi:10.1093/med/9780199696758.001.0001. ISBN   978-0-19-969675-8 . Retrieved 2015-09-07.
  19. ↑ Santisteban MM, Iadecola C, Carnevale D (January 2023). "Hypertension, neurovascular dysfunction, and cognitive impairment". Hypertension. 80 (1): 22–34. doi:10.1161/HYPERTENSIONAHA.122.18085. PMC   9742151 . PMID   36129176.
  20. ↑ Goldstein LB, Toth PP, Dearborn-Tomazos JL, Giugliano RP, Hirsh BJ, Peña JM, et al. (October 2023). "Aggressive LDL-C Lowering and the Brain: Impact on Risk for Dementia and Hemorrhagic Stroke: A Scientific Statement From the American Heart Association". Arteriosclerosis, Thrombosis, and Vascular Biology. 43 (10): e404–e442. doi:10.1161/ATV.0000000000000164. PMID   37706297.
  21. 1 2 van de Vorst IE, Vaartjes I, Geerlings MI, Bots ML, Koek HL (October 2015). "Prognosis of patients with dementia: results from a prospective nationwide registry linkage study in the Netherlands". BMJ Open. 5 (10): e008897. doi:10.1136/bmjopen-2015-008897. PMC   4636675 . PMID   26510729. Open Access logo PLoS transparent.svg
  22. ↑ Villarejo A, Benito-León J, Trincado R, Posada IJ, Puertas-Martín V, Boix R, et al. (2011). "Dementia-associated mortality at thirteen years in the NEDICES Cohort Study". Journal of Alzheimer's Disease. 26 (3): 543–51. doi:10.3233/JAD-2011-110443. PMID   21694455.
  23. ↑ Garcia-Ptacek S, Farahmand B, Kåreholt I, Religa D, Cuadrado ML, Eriksdotter M (2014). "Mortality risk after dementia diagnosis by dementia type and underlying factors: a cohort of 15,209 patients based on the Swedish Dementia Registry". Journal of Alzheimer's Disease. 41 (2): 467–77. doi: 10.3233/JAD-131856 . PMID   24625796.
  24. ↑ Fletcher, A (June 2023). "Good Practice Series No 11- MEs and Dementia". The Royal College of Pathologists. p. 8. Retrieved March 19, 2024.
  25. ↑ Wolters FJ, Ikram MA (2019). "Epidemiology of Vascular Dementia". Arteriosclerosis, Thrombosis, and Vascular Biology. 39 (8). Arterioscler Thromb Vasc Biol: 1542–1549. doi: 10.1161/ATVBAHA.119.311908 . PMID   31294622.
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