The DOI matches its Crossref record; 195 of the 196 references it cites were found in a registry or an index; none of the 57 sources its claims cite is checked for support yet.
The overlap between vascular disease and Alzheimer’s disease - lessons from pathology
Open accessAbstract
Recent epidemiological and clinico-pathological data indicate considerable overlap between cerebrovascular disease (CVD) and Alzheimer's disease (AD) and suggest additive or synergistic effects of both pathologies on cognitive decline. The most frequent vascular pathologies in the aging brain and in AD are cerebral amyloid angiopathy and small vessel disease. Up to 84% of aged subjects show morphological substrates of CVD in addition to AD pathology. AD brains with minor CVD, similar to pure vascular dementia, show subcortical vascular lesions in about two-thirds, while in mixed type dementia (AD plus vascular dementia), multiple larger infarcts are more frequent. Small infarcts in patients with full-blown AD have no impact on cognitive decline but are overwhelmed by the severity of Alzheimer pathology, while in early stages of AD, cerebrovascular lesions may influence and promote cognitive impairment, lowering the threshold for clinically overt dementia. Further studies are warranted to elucidate the many hitherto unanswered questions regarding the overlap between CVD and AD as well as the impact of both CVD and AD pathologies on the development and progression of dementia.
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TL;DR
This review synthesizes pathological and clinicopathological evidence that cerebrovascular disease (CVD) and Alzheimer’s disease (AD) frequently overlap, with additive or synergistic effects on cognitive decline. It emphasizes that vascular lesions may lower the threshold for dementia in early AD, while severe AD pathology often overwhelms the cognitive impact of small vascular lesions.
Key findings
- Up to 84% of aged subjects show morphological substrates of CVD in addition to AD pathology; cerebral amyloid angiopathy (CAA) is present in 82% to 98% of AD patients, and small vessel disease (SVD) is common in both aging and AD.
- In pure vascular dementia (VaD), about 68% of cases show lacunar/strategic subcortical infarcts and 32.5% show multiple large cortico-subcortical infarcts; in mixed dementia (AD + severe CVD), 56.6% show multiple large/lobar or cortico-subcortical lesions and 43.4% show small subcortical lacunar, micro-infarcts, or strategic infarcts.
- Small infarcts in full-blown AD have no impact on cognitive decline and are overwhelmed by Alzheimer pathology, whereas in early AD, cerebrovascular lesions may promote cognitive impairment and lower the threshold for clinically overt dementia.
- Converging autopsy, amyloid PET, functional MRI, and CSF biomarker evidence indicates that AD and CVD exert additive rather than interactive adverse effects on cognitive health, though interactions between vascular factors and amyloidosis/tauopathy remain unresolved.
Methods
- Narrative review of epidemiological, clinico-pathological, and autopsy studies on the overlap between CVD and AD, including data from large cohorts such as the National Alzheimer’s Coordinating Center (NACC) database and the Rush Memory and Aging Project/Religious Orders Study.
- The paper summarizes prevalence and topographical distribution of cerebrovascular lesions across AD, VaD, mixed dementia, and aged controls, using tables from prior autopsy series (e.g., VaD total 188; mixed dementia n = 83; NACC 5,715 autopsy cases).
- Main analysis is qualitative synthesis of reported frequencies, odds ratios, and clinicopathological correlations; no new primary data or systematic meta-analysis are presented.
Limitations
- The paper states that further studies are warranted to elucidate unanswered questions about CVD–AD overlap and that there is still a lack of consensus on incorporating vascular disease into clinical and neuropathological classification schemes for dementias.
- It notes that sample selection may strongly bias results: community samples tend to show greater cerebrovascular pathology than hospital-based samples, and mixed AD/CVD prevalence was higher in the community-based RUSH Memory and Aging Project (44%) than in the RUSH Religious Order Study (28%).
- The text also raises doubts about PiB-PET as representative of Aβ loads in the living brain and states that differentiation of mixed AD/CVD with CSF biomarkers may be difficult; evident from the text, this is a narrative review without a systematic search or quantitative pooling, so findings depend on heterogeneous autopsy cohorts and diagnostic criteria.
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![Figure 1 Pathogenic factors for the development of mixed dementia. Modified from [147].](/paper-figures/be2cadd94b8a4d16bf066e0aad0e12f5/the-overlap-between-vascular-disease-and-alzheimers-disease-lessons-from-figure-1.jpg)
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In the paper
“In AD brains with minor CVD the majority of CVLs are lacunar infarcts in basal ganglia and white matter, and multiple micro-infarcts.”
§ The overlap between vascular disease and Alzheimer’s disease - lessons from pathology > Review > Topographical distribution of cerebrovascular lesions
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“while in mixed type dementia (AD plus vascular dementia), multiple larger infarcts are more frequent.”
§ The overlap between vascular disease and Alzheimer’s disease - lessons from pathology > Abstract
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In the paper
“By contrast, mixed dementia (AD + severe CVD), according to our experience, is more frequently characterized by large or lobar infarcts, and multiple cortico-subcortical lesions (56.6%) than small subcortical lacunar infarcts, micro-infarcts, or strategic infarcts (43.4%, Table 2)”
§ The overlap between vascular disease and Alzheimer’s disease - lessons from pathology > Review > Topographical distribution of cerebrovascular lesions
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“AD brains with minor CVD, similar to pure vascular dementia, show subcortical vascular lesions in about two-thirds”
§ The overlap between vascular disease and Alzheimer’s disease - lessons from pathology > Abstract
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Up to 84% of aged subjects show morphological substrates of CVD in addition to AD pathology.”
§ The overlap between vascular disease and Alzheimer’s disease - lessons from pathology > Abstract
What the sources say
- Not checked yetcites [1] Petrovitch H, Ross GW, Steinhorn SC, Abbott RD, Markesberry W, Davis DG, Nelson J, Hardman J, Masaki KH, Vogt MR, Launer LJ, White LR: AD lesions and infarcts in demented and no-demented Japanese-American men. Ann Neurol. 2005, 57: 98-103. source
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None of the sources cited for this claim have been checked yet.
In the paper
“These data add further evidence for AD pathology (mainly neurofibrillary tangles and neuritic plaques) being the main morphological substrate of clinical dementia [51],[79],[80].”
§ The overlap between vascular disease and Alzheimer’s disease - lessons from pathology > Review > Coincidence between cerebrovascular disease and Alzheimer’s disease
What the sources say
- Not checked yetcites [51] Bennett DA, Wilson RS, Arvanitakis Z, Boyle PA, de Toledo-Morrell L, Schneider JA: Selected findings from the religious orders study and rush memory and aging project. J Alzheimers Dis. 2013, 33: S397-S403. source
- Not checked yetcites [79] Nelson PT, Jicha GA, Schmitt FA, Liu H, Davis DG, Mendiondo MS, Abner EL, Markesbery WR: Clinicopathologic correlations in a large Alzheimer disease center autopsy cohort: neuritic plaques and neurofibrillary tangles “do count” when staging disease severity. J Neuropathol Exp Neurol. 2007, 66: 1136-1146. source
- Not checked yetcites [80] Nelson PT, Pious NM, Jicha GA, Wilcock DM, Fardo DW, Estus S, Rebeck GW: APOE-epsilon2 and APOE-epsilon4 correlate with increased amyloid accumulation in cerebral vasculature. J Neuropathol Exp Neurol. 2013, 72: 708-715. source
plaindirect- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“while small CVLs alone, seen in 10% to 50% of aged cognitively unimpaired controls, are not likely to account for a single cause of dementia.”
§ The overlap between vascular disease and Alzheimer’s disease - lessons from pathology > Review > Topographical distribution of cerebrovascular lesions
hedged- Asserted: passes — The authors put it forward as true.
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In the paper
“However, AD pathology alone more frequently accounts for dementia than both macroscopic and microscopic infarcts [15]”
§ The overlap between vascular disease and Alzheimer’s disease - lessons from pathology > Review > Coincidence between cerebrovascular disease and Alzheimer’s disease
What the sources say
- Not checked yetcites [15] Troncoso JC, Zonderman AB, Resnick SM, Crain B, Pletnikova O, O’Brien RJ: Effect of infarcts on dementia in the Baltimore longitudinal study of aging. Ann Neurol. 2008, 64: 168-176. source
plaindirect- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“while in early stages of AD, cerebrovascular lesions may influence and promote cognitive impairment, lowering the threshold for clinically overt dementia.”
§ The overlap between vascular disease and Alzheimer’s disease - lessons from pathology > Abstract
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“The combination of two or more pathological processes may influence the severity of cognitive deficits, unmasking preclinical dementia due to mild AD lesions”
§ The overlap between vascular disease and Alzheimer’s disease - lessons from pathology > Review > Topographical distribution of cerebrovascular lesions
hedgedconditional- Asserted: passes — The authors put it forward as true.
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- It may state two separate claims as one. 7
- Probably not a substantial claim. 1
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Recent epidemiological and clinico-pathological data indicate considerable overlap between cerebrovascular disease (CVD) and Alzheimer’s disease (AD) and suggest additive or synergistic effects of both pathologies on cognitive decline.”
§ The overlap between vascular disease and Alzheimer’s disease - lessons from pathology > Abstract
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
In the paper
“There are considerable differences in the pathological burden in relation to age of onset of dementia, suggesting that late onset is associated with increased vascular pathology and lower AD burden [161],[162].”
§ The overlap between vascular disease and Alzheimer’s disease - lessons from pathology > Review > Cerebrovascular and Alzheimer’s disease pathology in demented and non-demented elderly
What the sources say
- Not checked yetcites [161],[162]
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“A lacunar state in basal ganglia and/or white matter was observed in 73%, hippocampal sclerosis in 3%, and mixed cerebral pathologies in 6%, whereas only 9% were free of CVLs [169].”
§ The overlap between vascular disease and Alzheimer’s disease - lessons from pathology > Review > Cerebrovascular and Alzheimer’s disease pathology in demented and non-demented elderly
What the sources say
- Not checked yetcites [169] Jellinger KA, Attems J: Neuropathology and general autopsy findings in nondemented aged subjects. Clin Neuropathol. 2012, 31: 87-98. source
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“The pathogenic chain of these and other deleterious effects, in a vicious circle, finally produces either structural cerebral disintegration (lacunes, infarcts, WMLs) with compromised neuronal metabolism, mitochondrial deficiency, oxidative stress, protein degradation, failure promoting cytoskeletal lesions with deposition of Aβ, and formation of neuritic lesions (e.g., neurofibrillary tangles).”
§ The overlap between vascular disease and Alzheimer’s disease - lessons from pathology > Review > Pathogenic factors
What the sources say
- Not checked yetcites [147] Jellinger KA, Attems J: Neuropathological evaluation of mixed dementia. J Neurol Sci. 2007, 257: 80-87. source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Microvascular changes in the aged brain and in AD induce impairment of cerebral perfusion, in particular decrease of regional blood flow, reduction of glucose transport and utilization, loss of vascular innervation with special impact on the cholinergic and transmitter deficits in AD [171], impairment of neurovascular regulation, ultrastructural changes in capillaries and basement membranes due to”
§ The overlap between vascular disease and Alzheimer’s disease - lessons from pathology > Review > Pathogenic factors
What the sources say
- Not checked yetcites [171] Roman GC, Kalaria RN: Vascular determinants of cholinergic deficits in Alzheimer disease and vascular dementia. Neurobiol Aging. 2006, 27: 1769-1785. source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“These factors induce brain atrophy with cognitive and memory impairment (Figure 1) [147], although the complex cascade of these and other noxious factors needs further elucidation.”
§ The overlap between vascular disease and Alzheimer’s disease - lessons from pathology > Review > Pathogenic factors
What the sources say
- Not checked yetcites [147] Jellinger KA, Attems J: Neuropathological evaluation of mixed dementia. J Neurol Sci. 2007, 257: 80-87. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Both hypertension and CAA are associated with an increased prevalence of CVLs [157]”
§ The overlap between vascular disease and Alzheimer’s disease - lessons from pathology > Review > Pathogenic factors
What the sources say
- Not checked yetcites [157] Jellinger KA, Attems J: Prevalence and pathogenic role of cerebrovascular lesions in Alzheimer’s disease. J Neurol Sci. 2005, 229-230: 37-41. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
In the paper
“CVD has been suggested to be an important cause of cognitive impairment in the elderly, both by itself or as a catalyst for the conversion of low-grade AD to overt dementia [186].”
§ The overlap between vascular disease and Alzheimer’s disease - lessons from pathology > Conclusions
What the sources say
- Not checked yetcites [186] Kalaria RN, Kenny RA, Ballard CG, Perry R, Ince P, Polvikoski T: Towards defining the neuropathological substrates of vascular dementia. J Neurol Sci. 2004, 226: 75-80. source
hedgedconditional- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
The authors state this as an assumption.
WMLs contribute to cognitive decline.
“and, thus, are assumed to contribute to cognitive decline [184].”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The cited source says what the claim attributes to it.
In the citing paper
“Studies have consistently found a positive epidemiological correlation between Alzheimer’s disease (AD) and cardiometabolic traits, yet the biological mechanisms behind this correlation is not well understood [1–4].”
From Multi-trait association studies discover pleiotropic loci between Alzheimer’s disease and cardiometabolic traits (2021) · cites this paper as [1]
The cited source says what the claim attributes to it.
In the citing paper
“Studies have consistently found a positive epidemiological correlation between Alzheimer’s disease (AD) and cardiometabolic traits, yet the biological mechanisms behind this correlation is not well understood [1–4].”
From Multi-trait association studies discover pleiotropic loci between Alzheimer’s disease and cardiometabolic traits (2021) · cites this paper as [1]
In the citing paper
“Moreover, the growing recognition of overlapping pathologies (e.g., Lewy body inclusions, TDP-43 pathology, vascular lesions, etc.) among dementia patients indicates a wide range of biological heterogeneity within AD that necessitates a broader approach to scientific investigations of its pathophysiology [37–39].”
From Systems-based proteomics to resolve the biology of Alzheimer’s disease beyond amyloid and tau (2021) · cites this paper as [38]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
“Multiple infarcts (61 = 32.5%)”
§ The overlap between vascular disease and Alzheimer’s disease - lessons from pathology > Review > Topographical distribution of cerebrovascular lesions
Reported 61 · recomputed 58
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
§ The overlap between vascular disease and Alzheimer’s disease - lessons from pathology > Review > Topographical distribution of cerebrovascular lesions
“Table: Table 3 Common lesions in AD, VaD, MIX, and aged controls (from[130])”
§ The overlap between vascular disease and Alzheimer’s disease - lessons from pathology > Review > Topographical distribution of cerebrovascular lesions
“The type and average prevalence of CVLs in AD, VaD, mixed dementia, and aged controls is shown in Table 3[147].”
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
§ The overlap between vascular disease and Alzheimer’s disease - lessons from pathology > Review > Cerebrovascular and Alzheimer’s disease pathology in demented and non-demented elderly
“compared to 66.8% in age-matched controls, all showing low Braak stages (P <0.01).”
§ The overlap between vascular disease and Alzheimer’s disease - lessons from pathology > Review > Cerebrovascular and Alzheimer’s disease pathology in demented and non-demented elderly
“Minor and moderate vascular pathology in AD were about twice as frequent as in controls (26.2% vs. 12.2% and 20.9% vs. 11.3%; P <0.01). On the other hand, severe vascular pathology did not significantly differ between both groups (10.2% vs. 12.2%).”
Citations
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Background
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“Pathological studies show that AD and cardiovascular pathologies commonly co-exist (14).”
BackgroundRelationship between Hearing Loss and Dementia Differs According to the Underlying Mechanism
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BackgroundA typology of cerebral small vessel disease based on imaging markers
Sperber, C., Hakim, A., Gallucci, L., Seiffge, D. J., Rezny‐Kasprzak, B., Jäger, E., Meinel, T. R., Wiest, R., Fischer, U., Arnold, M., et al. (2023) · Journal of Neurology · doi:10.1007/s00415-023-11831-x · Cited by 11
“Cerebral small vessel disease (SVD) has been identified to cause numerous neurological and neuropsychiatric pathologies, including stroke [1], dementia [2, 3], depression [4], and motor disability [5].”
BackgroundContextualizing the Role of Osteopontin in the Inflammatory Responses of Alzheimer’s Disease
Lalwani, R. C., Volmar, C., Wahlestedt, C., Webster, K. A., & Shehadeh, L. A. (2023) · Biomedicines · doi:10.3390/biomedicines11123232 · Cited by 13
“…A β egress into the circulation via two-way transport systems such as the LDLR associated factors that circumvent the blood–brain barrier (BBB) [89,90] may contribute to AD progression by interfering with the clearance of A β by microglia, triggering tau hyperphosphorylation and the spread of…”
BackgroundAssociations between vascular health, brain stiffness and global cognitive function
Pavuluri, K., Huston, J., Ehman, R. L., Manduca, A., Jack, C. R., Senjem, M. L., Vemuri, P., & Murphy, M. C. (2024) · Brain Communications · doi:10.1093/braincomms/fcae073 · Cited by 15
“13,14 14-16 Recent advances in neuroimaging, neuropathology, epidemiology and genetics have expedited the understanding of the relationship between vascular injury and cognitive function.”
BackgroundGaur, A., Gallagher, D., Herrmann, N., Chen, J. J., Marzolini, S., OH, P. I., Amemiya, Y., Seth, A. K., Kiss, A., & Lanctôt, K. L. (2024) · Journal of Geriatric Psychiatry and Neurology · doi:10.1177/08919887241254469 · Cited by 11
“5-10 Yet, there is increasing evidence of high co-morbidity between AD and cerebrovascular disease, 11-16 which highlights the importance of investigations focused on the neurobiological underpinnings of vascular cognitive impairment.”
Can the Treatment of Hypertension in the Middle-Aged Prevent Dementia in the Elderly?
Coca, A., Monteagudo-Gimeno, E., Doménech, M., Camafort, M., & Sierra, C. (2016) · High Blood Pressure & Cardiovascular Prevention · doi:10.1007/s40292-016-0144-5 · Cited by 11
“However, emerging evidence supports the view that vascular risk factors and disorders may be also involved in AD [10–12].”
BackgroundUmlauf, E., Rappold, E., Schiller, B., Fuchs, P., Rainer, M. K., Wolf, B., & Zellner, M. (2016) · Oncotarget · doi:10.18632/oncotarget.9773 · Cited by 11
Malek‐Ahmadi, M. H., Chen, K., Perez, S. E., & Mufson, E. J. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-180765 · Cited by 11
“Although parenchymal amyloid deposition and CAA co-occur at a high rate [3–5, 9, 10], others report that individuals with severe CAA had significantly lower diffuse plaque loads than those without CAA suggesting that parenchymal and vascular amyloid clearance mechanisms may be independent processes…”
Identifying common disease trajectories of Alzheimer’s disease with electronic health records
Fu, M., Sankararaman, S. S., Paşaniuc, B., et al. (2025) · EBioMedicine · doi:10.1016/j.ebiom.2025.105831 · Cited by 10
Marquié, M., García‐Sánchez, A., Alarcón‐Martín, E., Martínez, J., Castilla-Martí, M., Castilla‐Martí, L., Orellana, A., Montrreal, L., de Rojas, I., García‐González, P., et al. (2023) · Frontiers in Neuroscience · doi:10.3389/fnins.2023.1076177 · Cited by 10
“As brain vascular lesions are very common in the elderly (Gorelick et al., 2011; Attems and Jellinger, 2014) and an important contributor to cognitive decline (Sweeney et al.”
BackgroundLiu, Z., Liu, L., Heidel, R. E., & Zhao, X. (2024) · Smart Health · doi:10.1016/j.smhl.2024.100478 · Cited by 12
Defining Alzheimer’s Disease through Proteomic CSF Profiling
Peña‐Bautista, C., Álvarez‐Sánchez, L., Balaguer, Á., Raga, L., García, L., Baquero, M., & Cháfer‐Pericás, C. (2024) · Journal of Proteome Research · doi:10.1021/acs.jproteome.4c00590 · Cited by 13
Lee, N. K., Kim, H., Chang, J. W., Jang, H., Kim, H., Yang, J., Kim, J., Son, J. P., & Na, D. L. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21155524 · Cited by 10
“Many groups support the notion that a considerable overlap exists between cerebrovascular disease and AD [2,3].”
BackgroundSurvival, cognitive functions, and brain MRI in patients with cSVD: 5-year observation
Добрынина, Л. А., Gadzhieva, Z. S., Kremneva, E. I., Витальевна, Ш. К., Tsypushtanova, M. M., Геннадьевна, М. А., Trubitsyna, V. V., Bitsieva, E. T., Filatov, A. S., Byrochkina, A. A., et al. (2022) · Annals of Clinical and Experimental Neurology · doi:10.54101/acen.2022.4.3 · Cited by 12
Reuck, J. D., Auger, F., Durieux, N., Deramecourt, V., Maurage, C., Cordonnier, C., Pasquier, F., Leys, D., & Bordet, R. (2017) · Folia Neuropathologica · doi:10.5114/fn.2017.66711 · Cited by 11
Jang, J., Park, J. H., Kim, S., Park, Y. H., Pyun, J., Lim, J., Kim, Y., Youn, Y. C., Kim, S., & Initiative, T. A. D. N. (2018) · PLoS ONE · doi:10.1371/journal.pone.0201852 · Cited by 10
Tau reduction in aged mice does not impact Microangiopathy
Bennett, R. E., Hu, M., Fernandes, A. R., Pérez-Rando, M., Robbins, A. B., Kamath, T. V., Dujardin, S., & Hyman, B. T. (2020) · Acta Neuropathologica Communications · doi:10.1186/s40478-020-01014-4 · Cited by 11
Research on the Glial–Lymphatic System and Its Relationship With Alzheimer’s Disease
Ding, D., Wang, X., Li, Q., Li, L., & Wu, J. W. (2021) · Frontiers in Neuroscience · doi:10.3389/fnins.2021.605586 · Cited by 11
“The characteristic pathological changes in AD include senile plaques, neuron fiber tangles, and extensive neuronal loss, while the pathogenesis is not completely clear (Attems and Jellinger, 2014), involving the Aβ cascade hypothesis, the tau protein abnormal modification hypothesis, the cholinergic injury hypothesis,…”
BackgroundLan, Y.-T., Blacker, D., Yuan, C., Chibnik, L. B., Albert Hofman, D., & Ma, Y. (2021) · Journal of Alzheimer s Disease · doi:10.3233/jad-210625 · Cited by 10
“Giving the shared modifiable risk factors for cardiovascular diseases and dementia [16–18] and the considerable overlaps between cerebrovascular and Alzheimer’s disease pathology [19], large visit-to-visit metabolic fluctuation may have a role in risk for cognitive decline as well.”
BackgroundPharmacological interventions for apathy in Alzheimer's disease
Ruthirakuhan, M. T., Herrmann, N., Abraham, E. H., & Lanctôt, K. L. (2016) · Cochrane Database of Systematic Reviews · doi:10.1002/14651858.cd012197 · Cited by 10
High Morning and Bedtime Home Blood Pressures Strongly Predict for Post-Stroke Cognitive Impairment
Yamamoto, Y., Nagakane, Y., Tomii, Y., & Akiguchi, I. (2016) · Journal of Stroke and Cerebrovascular Diseases · doi:10.1016/j.jstrokecerebrovasdis.2016.04.001 · Cited by 10
Cognitive Outcomes of Cardiovascular Surgical Procedures in the Old: An Important but Neglected Area
Keage, H. A. D., Smith, A. E., Loetscher, T., & Psaltis, P. J. (2016) · Heart Lung and Circulation · doi:10.1016/j.hlc.2016.09.002 · Cited by 10
Age-specific and gender-dependent impact of primary headache disorders on dementia risk
Yin, J., Tsai, C., Lee, P.-J., Chou, C.-H., Chen, S., Chung, C., Chien, W., Lin, C., Sung, Y., Yang, F., et al. (2018) · Medicine · doi:10.1097/md.0000000000013789 · Cited by 12
Ó’Caoimh, R., Gao, Y., Svendrovski, A., Illario, M., Iaccarino, G., Doğu, B. B., Kehoe, P. G., & Molloy, D. W. (2019) · Journal of Alzheimer s Disease · doi:10.3233/jad-180774 · Cited by 10
“The co-existence of AD and minor cerebrovascular changes is common, does not appear to affect rate of progression [53] and is often acceptable for inclusion in trials of AD where it does not affect the diagnostic classification [54].”
Soldan, A., Wang, J., Pettigrew, C. A., Davatzikos, C. A., Erus, G., Hohman, T. J., Dumitrescu, L. C., Bilgel, M., Resnick, S. M., Rivera‐Rivera, L. A., et al. (2024) · Brain Communications · doi:10.1093/braincomms/fcae276 · Cited by 10
MacKenzie, J. L., Ivanova, N., Nell, H. J., Giordano, C. R., Terlecky, S. R., Agca, C., Ağca, Y., Walton, P. A., Whitehead, S. N., & Cechetto, D. F. (2022) · Neuroscience · doi:10.1016/j.neuroscience.2022.01.026 · Cited by 9
“2014)and clinicopathological studies (Snowdon, 1997; Kalaria, 2000; Del Ser et al., 2005; Schneider et al., 2007; Cechetto et al., 2008; Toledo et al., 2013; Attems and Jellinger, 2014)and further supported by findings from research animal models (Whitehead et al.”
Gyllenhammar, M., Rennie, A., Padilla, D. F., Wallert, J., Rydström, A., Wahlund, L., Eriksdotter, M., Westman, E., & Ekman, U. (2023) · Journal of Alzheimer s Disease · doi:10.3233/jad-220741 · Cited by 10
“There is partial clinical and pathophysiological overlap between AD and VaD regarding, for example, subcortical vascular lesions and specific cognitive domain deficits [16, 17].”
BackgroundPhilbert, S. A., Xu, J., Scholefield, M., Patassini, S., Church, S. J., Unwin, R. D., Roncaroli, F., & Cooper, G. J. S. (2023) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2023.1215637 · Cited by 8
“Concomitant small vessel disease is often present with AD pathology; thus, highlighting the high degree of pathogenic overlap between the two diseases (Deramecourt et al., 2012; Attems and Jellinger, 2014).”
BackgroundXu, X., Zhang, C., Tang, G., Wang, N., & Feng, Y. (2024) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2023.1328979 · Cited by 9
Fu, H., Li, J., Zhang, C., et al. (2024) · Neuroscience Bulletin · doi:10.1007/s12264-023-01175-x · Cited by 9
“Genetics and metabolic risk factors that increase AD risks are also frequently linked to vascular health [10, 20, 21].”
Multi-pathological contributions toward atrophy patterns in the Alzheimer’s disease continuum
Mohanty, R., Ferreira, D., & Westman, E. (2024) · Frontiers in Neuroscience · doi:10.3389/fnins.2024.1355695 · Cited by 9
Risk factors for the neurodegenerative dementias in the Western Pacific region
Clarke, A. J., Brodtmann, A. G., Irish, M., Mowszowski, L., Radford, K. A., Naismith, S. L., Mok, V., Kiernan, M. C., Halliday, G. M., & Ahmed, R. M. (2024) · The Lancet Regional Health - Western Pacific · doi:10.1016/j.lanwpc.2024.101051 · Cited by 9
“Given the substantial clinicopathological overlap between AD and vascular dementia and their synergistic risk factor pro fi le, 19 we will discuss these subtypes collectively, drawing on insights from the recent Lancet Commission on Dementia Prevention, Intervention and Care.”
BackgroundOsborn, K. E., Alverio, J., Dumitrescu, L. C., Pechman, K. R., Initiative, A. D. N., Gifford, K. A., Hohman, T. J., Blennow, K., Zetterberg, H., & Jefferson, A. L. (2019) · Journal of Alzheimer s Disease · doi:10.3233/jad-190077 · Cited by 9
“another and compromise the aging brain in a synergistic manner [13].”
Pires, E. N. S., Ferreira, S. T., & Linden, R. (2020) · Journal of Neurochemistry · doi:10.1111/jnc.15129 · Cited by 9
“Coexisting neuropathological markers of AD and CVD are found at autopsy in the majority of brains in many cohorts of patients clinically diagnosed with AD (Attems & Jellinger, 2014; James et al., 2016).”
BackgroundLi, W., Li, Y., Qiu, Q., Sun, L., Yue, L., Li, X., & Xiao, S. (2019) · Frontiers in Endocrinology · doi:10.3389/fendo.2019.00827 · Cited by 9
Sarfo, F. S., Akinyemi, R., Howard, G., Howard, V. J., Wahab, K., Cushman, M., Levine, D. A., Ogunniyi, A. O., Unverzagt, F., Owolabi, M. O., et al. (2020) · Journal of the Neurological Sciences · doi:10.1016/j.jns.2020.116754 · Cited by 8
Stracke, S., Lange, S., Bornmann, S., Kock, H., Schulze, L. N., Klinger-König, J., Böhm, S., Vogelgesang, A., von Podewils, F., Flöel, A., et al. (2020) · Journal of Clinical Medicine · doi:10.3390/jcm9061919 · Cited by 9
“Importantly, clinical, pathological and epidemiological data point to a relevant overlap between cerebrovascular disease (CVD) and Alzheimer’s clinical syndrome [17].”
BackgroundBeishon, L., Panerai, R. B., Robinson, T. G., & Haunton, V. J. (2021) · Physiological Measurement · doi:10.1088/1361-6579/ac1185 · Cited by 9
Stanley, M. C., Poupore, N. S., Knisely, K., Miller, A., Imeh‐Nathaniel, A., Roley, L. T., Nathaniel, S. I., Goodwin, R. L., & Nathaniel, T. I. (2023) · Frontiers in Dementia · doi:10.3389/frdem.2023.1137856 · Cited by 9
“Vascular dementia (VaD), Alzheimer’s disease (AD), andMixed Vascular-Alzheimer’s Dementia (MVAD) are neurodegenerative cognitive disorders that have a variety of effects on each individual (Attems and Jellinger, 2014).”
BackgroundLennon, M. J., Karvelas, N., Ganesh, A., Whitehead, S. N., Sorond, F. A., Laforet, V. D., Head, E., Arfanakis, K., Kolachalama, V. B., Liu, X., et al. (2025) · GeroScience · doi:10.1007/s11357-025-01746-y · Cited by 10
“This is critical because it is increasingly reported that dementia risk increases as the number of brain pathologies increases, e.g., coexisting AD pathology and vascular pathology nearly doubles the risk of clinical dementia compared to AD pathology alone [4].”
Lee, J. S., Lee, H., Park, S., Choe, Y. S., Park, Y. H., Cheon, B. K., Hahn, A., Ossenkoppele, R., Kim, H. J., Kim, S., et al. (2020) · Neurology · doi:10.1212/wnl.0000000000010811 · Cited by 8
Daño vascular y rendimiento cognitivo-funcional en una población con deterioro cognitivo leve
Labos, E., Guajardo, M. E., Söderlund, M. E., Pagotto, V. L., Sagues, X., Seinhart, D. B., & Schapira, M. C. (2022) · Revista de Neurología · doi:10.33588/rn.7407.2021411 · Cited by 9
“La coexistencia de los dos tras-tornos, denominada demencia mixta, puede ser más común que la enfermedad de Alzheimer ‘pura’ o el trastorno cognitivo vascular ‘puro’ [2].”
BackgroundEgle, M. S., Deal, J. A., Walker, K. A., Wong, D. F., Sharrett, A. R., & Gottesman, R. F. (2024) · Alzheimer s Research & Therapy · doi:10.1186/s13195-024-01461-4 · Cited by 9
“Several pathological studies further demonstrated that a large proportion of patients with dementia have mixed [29, 30].”
BackgroundTau Protein as a Biological Fluid Biomarker in Neurodegenerative Dementias
Llorens, F., Villar‐Piqué, A., Candelise, N., Ferrer, I., & Zerr, I. (2019) · IntechOpen eBooks · doi:10.5772/intechopen.73528 · Cited by 10
“Additionally, studies in VaD cases may have selection bias as co-occurrence of vascular and AD-related pathology is well-known [53].”
BackgroundRisk factors of male and female Alzheimer's disease patients with neuropsychiatric symptoms
Broughton, P., Niles, A., Imeh‐Nathaniel, A., Nathaniel, S. I., Goodwin, R. L., Roley, L. T., & Nathaniel, T. I. (2024) · Geriatric Nursing · doi:10.1016/j.gerinurse.2024.11.001 · Cited by 8
Dementia Risk Due to Traumatic Brain Injury in Subtypes of Dementia in the Welsh Population
Simmonds, E., Han, J., Kirov, G., Sharp, D. J., Massey, T. H., & Escott‐Price, V. (2025) · Neurology · doi:10.1212/wnl.0000000000213866 · Cited by 7
Kachouei, A. A., Singar, S., Wood, A., Flatt, J. D., Rosenkranz, S. K., Rosenkranz, R. R., & Akhavan, N. S. (2025) · Nutrients · doi:10.3390/nu17142328 · Cited by 11
“There is a substantial body of evidence that supports the connections between CVDs and AD [10–12].”
Rethinking early Alzheimer’s disease: An impaired internal model updating disorder?
Antonioni, A. (2026) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2026.106790 · Cited by 8
Hayden, E. Y., Huang, J., Charreton, M., Nuñez, S., Putman, J. N., Teter, B., Lee, J. T., Welch, A. E., Frautschy, S. A., Cole, G. M., et al. (2020) · Translational Stroke Research · doi:10.1007/s12975-020-00786-0 · Cited by 7
Tsentidou, G., Μoraitou, D., & Tsolaki, M. (2022) · International Journal of Environmental Research and Public Health · doi:10.3390/ijerph192013366 · Cited by 8
Solé, M., Marazuela, P., Castellote, L., Bonaterra‐Pastra, A., Giménez‐Llort, L., & Hernández‐Guillamón, M. (2023) · British Journal of Pharmacology · doi:10.1111/bph.16065 · Cited by 8
“Because cerebrovascular dysfunction is an independent factor contributing to neurological impairment in AD (Attems & Jellinger, 2014), it would be expected that improved vascular condition could better maintain or recover neuronal performance.”
BackgroundAre Ischemic Stroke and Alzheimer’s Disease Genetically Consecutive Pathologies?
Filippenkov, I. B., Владимирович, Х. А., Mozgovoy, I. V., Dergunova, L. V., & Limborska, S. A. (2023) · Biomedicines · doi:10.3390/biomedicines11102727 · Cited by 7
“As a result, there are some similarities between the pathological phenotypes [26].”
BackgroundUnhealthy white matter connectivity, cognition, and racialization in older adults
Royse, S. K., Snitz, B. E., Hengenius, J. B., Huppert, T. J., Roush, R. E., Ehrenkranz, R. C., Wilson, J. D., Bertolet, M. H., Reese, A. C., Cisneros, G., et al. (2023) · Alzheimer s & Dementia · doi:10.1002/alz.13494 · Cited by 6
“9 WMH and AD pathology also often regionally co-occur.”
BackgroundInteraction Between Arteriosclerosis and Amyloid-β on Cognitive Function
Frentz, I., van Arendonk, J., Leeuwis, A. E., Vernooij, M. W., van der Flier, W. M., Bos, D., Deyn, P. P. D., Wolters, F. J., & Ikram, M. A. (2024) · Journal of Alzheimer s Disease · doi:10.3233/jad-230604 · Cited by 7
Holz, M. R., Kochhann, R., Ferreira, P. C. D. S., Tarrasconi, M., Chaves, M. L. F., & Fonseca, R. P. (2017) · Dementia & Neuropsychologia · doi:10.1590/1980-57642016dn11-040013 · Cited by 7
Physical Performance in Memory Clinic Patients: The Potential Role of the White Matter Network
Verwer, J., Reijmer, Y., Koek, H., Biessels, G., Exalto, L., Groeneveld, O., Heinen, R., Heringa, S., Kalsbeek, N., Maher, C., et al. (2019) · Journal of The American Geriatrics Society · doi:10.1111/jgs.15987 · Cited by 6
“However, this does reflect clinical practice as, in a memory clinic setting, vascular brain injury commonly co-occurs with other pathologies.(7) The current findings are likely to be generalizable to other memory clinic patients.”
BackgroundДобрынина, Л. А., Gadzhieva, Z. S., Akhmetzyanov, B. M., Kalashnikova, L. A., & Кротенкова, М. В. (2019) · S S Korsakov Journal of Neurology and Psychiatry · doi:10.17116/jnevro201911912281 · Cited by 7
Impact of Alzheimer's disease and related dementia diagnosis following treatment for bladder cancer
Jazzar, U., Shan, Y., Klaassen, Z. W. A., Freedland, S. J., Kamat, A. M., Raji, M. A., Masel, T., Tyler, D. S., Baillargeon, J., Kuo, Y., et al. (2020) · Journal of Geriatric Oncology · doi:10.1016/j.jgo.2020.04.009 · Cited by 7
Beishon, L., Panerai, R. B., Budgeon, C. A., Subramaniam, H., Mukaetova-Ladinska, E. B., Robinson, T. G., & Haunton, V. J. (2021) · Journal of Alzheimer s Disease · doi:10.3233/jad-201444 · Cited by 7
Schoemaker, D., Velilla-Jiménez, L. M., Zuluaga, Y., Baena, A. Y., Ospina, C., Bocanegra, Y., Álvarez, S., Ochoa‐Escudero, M., Guzmán‐Vélez, E., Martinez, J. E., et al. (2021) · Journal of Alzheimer s Disease · doi:10.3233/jad-210313 · Cited by 7
Priemer, D. S., & Folkerth, R. D. (2021) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlab059 · Cited by 7
VAMP2 Expression and Genotype Are Possible Discriminators in Different Forms of Dementia
Costa, A. S., Ferri, E., Guerini, F. R., Rossi, P. D., Arosio, B., & Clerici, M. (2022) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2022.858162 · Cited by 8
Li, M., Qu, K., Wang, Y., Wang, Y., & Sun, L. (2023) · Journal of Hypertension · doi:10.1097/hjh.0000000000003593 · Cited by 9
Tu, M.-C., Huang, S., Hsu, Y., Yang, J., Lin, C.-Y. E., & Kuo, L. (2024) · Scientific Reports · doi:10.1038/s41598-024-52910-x · Cited by 7
Roussotte, F. F., Siddarth, P., Merrill, D. A., Narr, K. L., Ercoli, L. M., Martinez, J., Emerson, N. D., Barrio, J. R., & Small, G. W. (2017) · American Journal of Geriatric Psychiatry · doi:10.1016/j.jagp.2017.09.001 · Cited by 7
“INTRODUCTION Recent epidemiological and clinico-pathological data demonstrate considerable overlap between cerebrovascular disease and Alzheimer’s disease (AD), and indicate that vascular and AD-type pathologies are leading causes of cognitive impairment in the elderly (1).”
Prevalence of cardiovascular drug use before and after diagnosis of Alzheimer's disease
Vu, M., Koponen, M., Taipale, H. T., Tanskanen, A. J., Tiihonen, J., Kettunen, R., Hartikainen, S. A., & Tolppanen, A. (2019) · International Journal of Cardiology · doi:10.1016/j.ijcard.2019.09.036 · Cited by 8
3D Mapping of Neurofibrillary Tangle Burden in the Human Medial Temporal LobePreprint
Yushkevich, P. A., Muñoz, M., Martin, M. M. I. D. O., Ittyerah, R., Lim, S., Ravikumar, S., Bedard, M. L., Pickup, S., Liu, W., Wang, J., et al. (2021) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2021.01.15.421909 · Cited by 7
“Most patients diagnosed with AD at autopsy also harbor one or more concomitant neurodegenerative pathologies, such as TDP-43 and asynuclein proteinopathies, non-AD tauopathies, as well as vascular disease [63, 36, 70, 7, 60, 75, 40, 55].”
BackgroundXie, G., Jiang, G., Huang, L., Sun, S., Wan, Y., Li, F., Wu, B., Zhang, Y., Li, X., Xiong, B., et al. (2025) · Pharmaceuticals · doi:10.3390/ph18060790 · Cited by 10
“In clinical practice, mixed dementia accounts for more than ~70% of cases [237,238].”
Lohner, V., Badhwar, A., Detcheverry, F. E., García, C. L., Gellersen, H. M., Khodakarami, Z., Lattmann, R., Li, R., Low, A., Mazo, C., et al. (2025) · Alzheimer s Research & Therapy · doi:10.1186/s13195-025-01815-6 · Cited by 7
“It is therefore expected that CSVD co-occurs and interacts with AD as well as other neurodegenerative disorders [108–113].”
Davey, D. A. (2015) · Journal of Alzheimer’s Disease & Parkinsonism · doi:10.4172/2161-0460.1000184 · Cited by 6
“The changes of AD and CVD overlap and both pathologies have both additive and synergistic effects on cognitive decline [13].”
BackgroundContribution of Peripheral Microvascular Dysfunction to Mild Cognitive Impairment
Gold, M. E., Rogers, S. C., Kulshreshtha, A., et al. (2024) · The American Journal of Cardiology · doi:10.1016/j.amjcard.2024.02.038 · Cited by 6
Associations of cardiac function and arterial stiffness with cerebrovascular disease
Tan, C. H., & Tan, J. J. X. (2024) · International Journal of Cardiology · doi:10.1016/j.ijcard.2024.132037 · Cited by 6
Gainey, M., Niles, A., Nathaniel, S. I., Goodwin, R. L., Roley, L. T., Win, O., Nathaniel, T. I., & Imeh‐Nathaniel, A. (2024) · Geriatric Nursing · doi:10.1016/j.gerinurse.2024.04.019 · Cited by 6
Anti-RGMa neutralizing antibody ameliorates vascular cognitive impairment in mice
Yamamoto, M., Itokazu, T., Uno, H., Maki, T., Shibuya, N., & Yamashita, T. (2024) · Neurotherapeutics · doi:10.1016/j.neurot.2024.e00500 · Cited by 5
Experimental microembolism induces localized neuritic pathology in guinea pig cerebrum
Li, J., Cai, Y., Liu, F., Yang, L., Hu, X., Patrylo, P. P., Cai, H., Luo, X.-G., Xiao, D., & Yan, X.-X. (2015) · OncoTarget · doi:10.18632/oncotarget.3599 · Cited by 5
“com/oncotarget to differentiate clinically because of the many shared neuropathological and neurological manifestations [18].”
BackgroundMuscarinic M1 Receptor Coupling to G-protein is Intact in Parkinson’s Disease Dementia
Lee, J. H., Francis, P. T., Ballard, C. G., Aarsland, D., Kalaria, R. N., Wong, P. T. ‐., Chen, C., & Lai, M. K. P. (2016) · Journal of Parkinson s Disease · doi:10.3233/jpd-160932 · Cited by 6
“Furthermore, there has been growing appreciation of the patho-physiological interactions between cerebrovascular disease (CVD) and AD [8].”
Heterogeneous Disease Progression in a Mouse Model of Vascular Cognitive Impairment
Lee, N. K., Kim, H., Yang, J., Kim, J., Son, J. P., Jang, H., & Na, D. L. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21082820 · Cited by 6
Chiu, W. T., Lee, T. Y., Chan, L., Wu, D., Huang, L. K., Chen, D. Y. T., Lee, Y. T., Hu, C. J., & Hong, C. (2020) · Clinical Neurology and Neurosurgery · doi:10.1016/j.clineuro.2020.105959 · Cited by 6
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STRIVEing to describe small vessel disease
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“This has been shown in epidemiological, clinical, and pathological data [41].”
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Cerebrovascular and Neurodegenerative Pathologies in Long-Term Stable Mild Cognitive Impairment
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“There are different pathologies of cognitive decline, but recent epidemiological, clinical, and neuropathological data indicate considerable overlap between cerebrovascular disease and AD [6].”
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Sleep, pericyte subtypes and cognitive decline in adults with and without Alzheimer’s disease
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“42 TgCRND8 transgenic mice show depletion of mural cells, including pericytes, covering both arterioles and venules, which is accompanied by abnormalities of functional hyperaemia, with further aberrant morphology with pharmacological depletion of pericytes.”
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“…(FTLD-TDP43), limbic-predominant age-related TDP-43 encephalopathy-neuro-pathologic change (LATE-NC)), [29, 30, 45, 46] non-AD tau (e.g., FTLD-tau, argyrophilic grain disease (AGD)), [58] as well as vascular brain injury (VBI) [3] commonly coexist with ADNC as postmortem findings [12, 31, 33].”
Distinct cerebrovascular pathways underlying Alzheimer’s disease-related neurodegeneration
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“There is ongoing debate on independent versus synergistic relationship of AD and cerebrovascular pathologies [3, 36, 37].”
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“Cerebrovascular disease (CVD) may also contribute to LLD, and CVD has also been linked to AD [57, 58].”
Metadata
- Authors
- Attems, J., & Jellinger, K. A.
- Affiliations
- Newcastle University (GB)
- Medical University of Vienna (AT)
- Corresponding author
- Attems, Johannes
- Venue
- BMC Medicine
- Published
- 2014-11-11
- Volume
- 12
- Issue
- 1
- Pages
- 206-206
- ISSN
- 1741-7015 (ISSN-L)
- PMC
- PMC4226890
- OpenAlex
- W2043522411
- Cited by
- 739
- References
- 196
- Citations by year
- 2026: 55 · 2025: 79 · 2024: 73 · 2023: 66 · 2022: 61 · 2021: 71 · 2020: 91 · 2019: 70 · 2018: 53 · 2017: 44 · 2016: 53 · 2015: 19 · 2014: 3
- FWCI
- 5.49
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- BMC Medicine (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Newcastle University ePrints (Newcastle Univesity) (cc-by)
- Funders
- Alzheimer's Society
- National Institute for Health and Care Research
- Dunhill Medical Trust (R173/1110)
- Newcastle University (G0400074)
- Newcastle upon Tyne Hospitals NHS Foundation Trust
- Medical Research Council (G0400074)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Keywords
- Alzheimer's disease, cerebrovascular disease, cerebral amyloid angiopathy, cerebral small vessel disease, vascular dementia, mixed dementia, cognitive decline, dementia progression, subcortical infarcts
- MeSH terms
- Aging, Alzheimer Disease, Cerebrovascular Disorders, Humans
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