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.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
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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.
- Based: passes — The paper gives a reason why it holds.
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
Cites
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Background
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Chatterjee, A., Lee, S. Y., Diaz, V., Saloner, R., Sanderson‐Cimino, M. E., DeCarli, C. S., Maillard, P., Hinman, J. D., Vossel, K. A., Casaletto, K. B., et al. (2024) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2024.06.002 · Cited by 6
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Baker, J., & Schott, J. M. (2022) · Revue Neurologique · doi:10.1016/j.neurol.2022.03.001 · Cited by 5
Mendes, F. R., Leclerc, J. L., Liu, L., Kamat, P. K., Naziripour, A., Hernandez, D., Li, C., Ahmad, A. S., & Doré, S. (2020) · Journal of Alzheimer s Disease · doi:10.3233/jad-191069 · Cited by 5
Tank, R., Ward, J., Flegal, K. E., et al. (2021) · doi:10.31234/osf.io/cr69u · Cited by 5
Subtyping Alzheimer’s disease and Parkinson’s disease using longitudinal electronic health records
Lian, J., Fan, Z., Petrazzini, B. O., Fan, W., Rao, S., Yang, Q., Zeng, G., Ahmed, N., Mofrad, F. T., Wamil, M., et al. (2026) · Nature Aging · doi:10.1038/s43587-026-01085-3 · Cited by 7
“In AD, this was characterized by extensive hypertension and elevated APOE4 frequency, supporting the ‘mixed dementia’ construct, where vascular damage may potentiate amyloid toxicity 44,45 .”
Paratonia in Advanced Dementia: A Frequently Misunderstood Movement Disorder
Perri, G., Hobbelen, H. J. S. M., Cuppage, J., Naglie, G., Feldman, S., Khan, O. I., Ismail, F., Boulias, C., & Kleiner, G. (2026) · Journal of the American Medical Directors Association · doi:10.1016/j.jamda.2026.106284 · Cited by 4
The efficacy of divasa in the early recovery period of ischemic stroke
Мудрова, О. А., Schekolova, N. B., & Borikov, F. A. (2016) · S S Korsakov Journal of Neurology and Psychiatry · doi:10.17116/jnevro20161163248-53 · Cited by 4
Huang, S., Nunez, J., Toresco, D. L., Wen, C., Slotabec, L. A., Wang, H., Zhang, H., Rouhi, N., Adenawoola, M. I., & Li, J. (2025) · The FASEB Journal · doi:10.1096/fj.202402725rr · Cited by 4
“25,120 Therefore, CAA is not only a feature of aging and AD but is also closely associated with cerebrovascular events such as cerebral hemorrhage and stroke.”
Melazzini, L., Savoldi, F., Chessa, M., Vitali, P., Zanardo, M., Bertoldo, E. G., Fiolo, V., Griffanti, L., Carminati, M., Frigiola, A., et al. (2022) · Brain Imaging and Behavior · doi:10.1007/s11682-022-00629-6 · Cited by 4
“For this reason, the hypothesis of dementia as a cardiovascular-driven disease has been recently put forward (de Roos et al., 2017), supported by the increasing evidence of the often co-existing signs of cerebrovascular disease with findings of Alzheimer’s pathology (Attems & Jellinger, 2014).”
ResultWang, K., Zhou, Y., Su, S., Jin, X., Lei, L., Ma, H., Liu, A., & Yang, Y. (2025) · Social Psychiatry and Psychiatric Epidemiology · doi:10.1007/s00127-025-02837-z · Cited by 7
“Cardiovascular disease has been shown to promote the formation of neurofibrillary tangles, a characteristic feature of Alzheimer's disease, which in turn leads to cognitive dysfunction [33].”
Tripathi, S. M., McNeil, C. J., Staff, R. T., Murray, A. D., Wischik, C. M., Schelter, B. O., & Waiter, G. D. (2025) · Nuclear Medicine and Molecular Imaging · doi:10.1007/s13139-025-00908-2 · Cited by 4
“AD is frequently associated with cerebrovascular disease (CVD) and the presence of both pathologies has an additive impact on cognitive decline [1–3].”
Percy, M. E., & Lukiw, W. J. (2017) · International Journal of Developmental Disabilities · doi:10.1080/20473869.2017.1301023 · Cited by 4
“Brain studies have revealed vascular involvement in as many as two-thirds of dementia cases (Attems and Jellinger 2014).”
BackgroundBrain Network Functional Connectivity in Alzheimer’s Disease and Frontotemporal Dementia
Zhou, J. H., Ng, K. K., & Liu, S. (2020) · Springer eBooks · doi:10.1007/978-3-030-41874-8_25 · Cited by 4
Kim, H., Park, J., Kim, Y. S., & Park, J. (2020) · International Journal of Geriatric Psychiatry · doi:10.1002/gps.5458 · Cited by 5
Nag, N., Lin, X., Yu, M., Simpson, S., Jelinek, G. A., Neate, S. L., & Levin, M. (2021) · Journal of Personalized Medicine · doi:10.3390/jpm11020144 · Cited by 4
“Our findings showed inverse associations with all lifestyle behaviours for both AD and stroke, aligning with the latter being an established risk factor for all-cause dementia [42], and the recognized coincidence of cerebrovascular disease and AD [43].”
ResultBihaqi, S. W., Rao, H. V., Sen, A., & Grammas, P. (2021) · Cerebral Circulation - Cognition and Behavior · doi:10.1016/j.cccb.2021.100014 · Cited by 4
Treatment of Vascular and Neurodegenerative Forms of Cognitive Impairment and Dementias
Perlett, L., & Smith, E. E. (2022) · Clinics in Geriatric Medicine · doi:10.1016/j.cger.2022.07.008 · Cited by 5
Vascular Dementia: Definitions, Origins, Symptoms, Diagnosis and Treatments
Bourin, M. (2023) · SAR Journal of Psychiatry and Neuroscience · doi:10.36346/sarjpn.2023.v04i01.001 · Cited by 4
Pathogenic Angiogenic Mechanisms in Alzheimer's Disease
Singh, C. S. B., Pfeifer, C. G., & Jefferies, W. A. (2017) · InTech eBooks · doi:10.5772/66403 · Cited by 7
“Vascular pathologies that have been seen in the aged human brain include: cerebral amyloid angiopathy (CAA), cerebral atherosclerosis, small vessel disease in most cases caused by hypertensive vasculopathy or microvascular degeneration, blood‐brain barrier (BBB) dysfunction causing white matter lesions, microinfarctio…”
BackgroundKim, J. W., Byun, M. S., Yi, D., Lee, J. H., Ko, K., Jung, G., & Lee, D. Y. (2019) · Neuropsychiatric Disease and Treatment · doi:10.2147/ndt.s192231 · Cited by 4
Chibhabha, F., Yaqi, Y., & Li, F. (2020) · Reviews in the Neurosciences · doi:10.1515/revneuro-2019-0119 · Cited by 4
Carolis, A. D., Cipollini, V., Donato, N., Sepe‐Monti, M., Orzi, F., & Giubilei, F. (2016) · Neurological Sciences · doi:10.1007/s10072-016-2716-5 · Cited by 5
Hypertension, Cognitive Decline, and Dementia
Sierra, C., Vicario, A., & Escoda, O. (2016) · Updates in hypertension and cardiovascular protection · doi:10.1007/978-3-319-32074-8_15 · Cited by 4
Biomarkers of Alzheimer’s disease
Bos (2018) · Research Publications (Maastricht University) · doi:10.26481/dis.20181012ib · Cited by 4
Natural language processing and modeling of clinical disease trajectories across brain disordersPreprint
Mekkes, N., Groot, M., Wehrens, S. M. T., Hoekstra, E., Herbert, M. K., Brummer, M. L., Wever, D. D., Eggen, B. J. L., Rozemüller, A. J. M., Huitinga, I., et al. (2022) · medRxiv · doi:10.1101/2022.09.22.22280158 · Cited by 4
Integrative Spatial Omics for Systems-Level Mapping of Pathological NichesPreprint
Kruse, A. R. S., Lardenoije, R., Migas, L. G., Scott, C. F., Marshall, C. R., Malek, M. C., Eskaros, A., Pham, T. H., Aamodt, K. I., Colley, M. E., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.09.12.675904 · Cited by 6
“Both clusters contained molecules localized to islets (Figure S6).”
A Review on the Pathophysiology of Alzheimer’s Disease
Agarwal, U., Kapoor, G. T., & Tonk, R. K. (2025) · Current Protein and Peptide Science · doi:10.2174/0113892037416859250915091846 · Cited by 5
Kancheva, A. K., Lyall, D. M., Tsvetanov, K. A., Kancheva, I. K., Mavromati, K., Koychev, I. G., Tari, B., García, D. J., Hughes, L., Wardlaw, J. M., et al. (2025) · Journal of the American Heart Association · doi:10.1161/jaha.125.044438 · Cited by 3
“39 To address the possibility that the observed moderation effects reflected nonlinear rather than linear relationships, we examined model fit after adding quadratic terms for both biomarkers and ASCVD risk.”
Xu, F., Zhang, Y., Tan, D., He, Y., Fei, Q., & Xu, K. (2026) · Frontiers in Public Health · doi:10.3389/fpubh.2026.1793973 · Cited by 3
“Moreover, AD often coexists with vascular pathology (mixed dementia) (81).”
Zhao, L., Peng, T., & Wu, S. (2025) · Nanotechnology and nanomaterials. · doi:10.5772/intechopen.1008681 · Cited by 3
Lohkamp, K. J., Timmer, N., Guardia, G. S., Shenk, J. C., Verweij, V., Geenen, B., Dederen, P. J. W. C., Bakker, L., Egitimci, C., Yoldas, R., et al. (2025) · Life · doi:10.3390/life15030333 · Cited by 4
“In accordance with the literature, spatial learning deficits in the MWM are reported in APP/PS1 as early as 6 months of age and become more pronounced by 12 months of age [45,46].”
Early detection of Alzheimer’s disease using small RNAs. Results from the EPAD cohort
Sikosek, T., Heuvelman, M., Mika, J., Kahraman, M., Jehn, J., Frank, M., Daniel-Moreno, A., Ceiler, J., Skottke, J., Sánchez-Delgado, M., et al. (2025) · The Journal of Prevention of Alzheimer s Disease · doi:10.1016/j.tjpad.2025.100257 · Cited by 5
“Our findings also shed light on vascular contributions to AD pathology [ 55 , 56 ].”
Bommarito, G., Griffa, A., Michel, P., Caroline, H., Salvioni, C. P., Pistocchi, S., Alemán-Gómez, Y., Damian, D., Jreige, M., Prior John, O., et al. (2025) · Alzheimer s Research & Therapy · doi:10.1186/s13195-025-01805-8 · Cited by 4
“Pathological studies found HTNA features in 20–50% of AD patients [2, 3], and a high occurrence of CAA in DLB and AD patients [4, 5].”
Rosenich, E., & Lim, Y. Y. (2025) · Alzheimer s Research & Therapy · doi:10.1186/s13195-025-01776-w · Cited by 3
“Given that CVD is present in approximately 50–84% of individuals aged 80–90 + at autopsy [15, 19, 20], and is associated with an increased risk of progression to AD and vascular dementia, even after accounting for levels of Aβ and tau [7, 21–24], it is important to understand how hallmark AD…”
Dexmedetomidine and postoperative dementia risk in older patients
Sun, M., Fu, S., Tian, M., Li, W., Cai, S., Xie, X., Chen, W., Wu, S., & Zhang, J. (2025) · Age and Ageing · doi:10.1093/ageing/afaf258 · Cited by 4
Cheng, Z., Gao, F., Lv, X., Wang, Q., Wu, Y., Sun, B., & Shen, Y. (2022) · Journal of Alzheimer s Disease · doi:10.3233/jad-220872 · Cited by 3
Ortner, M., Lanz, K., Goldhardt, O., Müller‐Sarnowski, F., Diehl‐Schmid, J., Förstl, H., Hedderich, D. M., Yakushev, I. Y., Logan, C. A., Weinberger, J.-P., et al. (2023) · Journal of Alzheimer s Disease · doi:10.3233/jad-221187 · Cited by 4
“Vascular disease is thought to play a major role in the pathogenesis of AD [20].”
BackgroundKan, C. N., Huang, X., Zhang, L., Hilal, S., Reilhac, A., Tanaka, T., Venketasubramanian, N., Chen, C., & Xu, X. (2023) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2023.08.005 · Cited by 3
Wang, H., Zhang, Z., & Hongpaisan, J. (2023) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2023.1272361 · Cited by 3
“Alzheimer’s disease (AD) was previously described as non-vascular dementia (Kalaria and Ballard, 1999; Attems and Jellinger, 2014).”
BackgroundBello, M., Mammino, K., Vernon, M. A., Wakeman, D. G., Denmon, C., Krishnamurthy, L. C., Krishnamurthy, V., McGregor, K., Novak, T. S., & Nocera, J. R. (2024) · JMIR Research Protocols · doi:10.2196/58316 · Cited by 4
“In fact, recent epidemiological and clinicopathological data indicate considerable overlap between cerebrovascular dysfunction in aging and AD [2,3].”
BackgroundYu, R., Kong, S. D. X., Ireland, C., Steiner-Lim, G. Z., Bassett, K., Almgren, H., Wang, D., Wang, C., Michaelian, J. C., & Naismith, S. L. (2024) · Brain Behavior & Immunity - Health · doi:10.1016/j.bbih.2024.100924 · Cited by 4
“The most common forms of dementia are Alzheimer ’ s disease (AD) and vascular dementia (VaD), accounting for up to 70% and 20% of all cases respectively, though the majority of cases present with a mixed aetiology of both AD and VaD pathologies (Akhter et al., 2021; Attems and Jellinger, 2014).”
Peculiarities of Neurological Disorders and Study Designs
Beghi, E., Pupillo, E., & Giussani, G. (2016) · Monographs in clinical neuroscience/Frontiers of neurology and neuroscience/Monographs in neural sciences · doi:10.1159/000445409 · Cited by 3
Wajman, J. R. (2018) · International Journal of Brain and Cognitive Sciences · Cited by 3
Acquired Brain Injury Following Sepsis*
Hopkins, R. O. (2019) · Critical Care Medicine · doi:10.1097/ccm.0000000000003981 · Cited by 3
“Data in vascular brain injury has found that there are different mechanisms that are responsible for large vessel infarcts from the mechanisms that cause small vessel infarcts, as such the large infarcts may be independent of small vessel infarcts, although this needs to be verified in sepsis populations (15).”
BackgroundBrachial Flow-mediated Dilation and Risk of Dementia
Garg, P. K., Tan, A. X., Odden, M. C., et al. (2020) · Alzheimer Disease & Associated Disorders · doi:10.1097/wad.0000000000000394 · Cited by 3
“6 This substudy was continued for participants (through 2014) at the Pittsburgh site if they (1) were alive and did not have dementia in 1998-1999 and (2) had either a second magnetic resonance image and/or a detailed cognitive evaluation in 1998-1999 (n= 532).”
BackgroundMixed dementia in stroke patient
Cherdak, M. A. (2020) · Russian Journal of Geriatric Medicine · doi:10.37586/2686-8636-3-2020-236-242 · Cited by 3
Geerts, H., & van der Graaf, P. (2021) · Journal of Alzheimer s Disease Reports · doi:10.3233/adr-210039 · Cited by 3
“For instance, it has been reported that over 80% of AD brains show vascular pathology to some degree [1].”
BackgroundRobinson, J. L., Richardson, H., Xie, S. X., Alfaro, B., Loh, N., Lee, V. M. ‐., Lee, E. B., & Trojanowski, J. Q. (2022) · Free Neuropathology · doi:10.17879/freeneuropathology-2022-3792 · Cited by 3
An, L., Binette, A. P., Hristovska, I., Vilkaite, G., Xiao, Y., Zendehdel, R., Dong, Z., Smets, B., Saloner, R., Tasaki, S., et al. (2025) · medRxiv · doi:10.1101/2025.06.27.25330344 · Cited by 3
“This might indicate misdiagnosis, could be indicative of co-pathology 95 , or may even indicate a vascular etiology for a subgroup of AD patients 96,97 .”
Liang, J., Zhang, Y., Zhang, W., Pan, Y., Gao, D., Ma, J., Liu, Y., Dai, Y., Ji, M., Xie, W., et al. (2025) · The Journal of Prevention of Alzheimer s Disease · doi:10.1016/j.tjpad.2024.100041 · Cited by 2
Aiello, E. N., Curti, B., Luca, G. D., Trombi, M., Maranzano, A., Poletti, B., Silani, V., Ticozzi, N., & Verde, F. (2025) · Journal of Alzheimer s Disease · doi:10.1177/13872877251318011 · Cited by 2
“26 In fact, no systematic search for AD-related biomarkers was performed in VMCI/VD.”
Liakakis, G., Vakrakou, A. G., Boufidou, F., Constantinides, V. C., Velonakis, G., Paraskevas, G. P., Stefanis, L., & Kapaki, E. N. (2025) · Diagnostics · doi:10.3390/diagnostics15060669 · Cited by 3
“SSVD frequently coexists or favors the development of AD [3,4].”
From dark horse to front-runner: vascular contributions to brain health
Gupta, A., Pires, P. W., Billinger, S. A., et al. (2025) · GeroScience · doi:10.1007/s11357-025-01840-1 · Cited by 2
“Notwithstanding, autopsy studies suggest that 80–90% of brains affected with Alzheimer’s disease have concomitant evidence of cerebrovascular disease pathologies and sequalae [2–4].”
Alkam, T., Tarshizi, E., & Benschoten, A. H. V. (2025) · Journal of Alzheimer s Disease Reports · doi:10.1177/25424823251392474 · Cited by 2
Wang, R., Gao, Y., Ee, N., Akinyede, F., Xu, X., Chen, L., Xiong, S., Chen, X., Anderson, C. S., Harris, K., et al. (2026) · The Journal of Prevention of Alzheimer s Disease · doi:10.1016/j.tjpad.2026.100500 · Cited by 2
“While, mixed dementia aetiology is common in late life, and clinical dementia subtypes often do not reflect a single underlying pathology because dementia pathology frequently overlaps [45].”
New perspectives on VEGF signalling in Alzheimer's disease
Emery, C. E. G., Love, S., & Miners, J. S. (2026) · Brain Pathology · doi:10.1111/bpa.70100 · Cited by 3
“…common and overlapping pathological features (reviewed [99 – 101]) with up to 84% of brains from elderly people having both vascular and AD pathology [102] — the presence of vascular pathology in AD is likely to contribute significantly to CSF and serum PlGF expression in AD and mixed dementia.”
Microglial Plasticity in Vascular Dementia: Mechanisms and Therapeutic Reprogramming
Shukla, M., Li, J., Sun, Y., Jin, R., & Li, G. (2026) · International Journal of Molecular Sciences · doi:10.3390/ijms27093719 · Cited by 3
Fitri, F. I., & Simanjuntak, P. (2023) · Jurnal Kedokteran Brawijaya · doi:10.21776/ub.jkb.2022.032.03.6 · Cited by 2
Добрынина, Л. А., Tsypushtanova, M. M., Шабалина, А. А., Витальевна, Ш. К., Геннадьевна, М. А., Trubitsyna, V. V., Bitsieva, E. T., Byrochkina, A. A., & Geints, A. A. (2023) · Annals of Clinical and Experimental Neurology · doi:10.54101/acen.2023.3.3 · Cited by 3
“Актуальность дан-ной проблемы повышается в связи с данными последних патологических исследований о том, что «чистые» формы ЦМА и БА уступают первенство смешанным, на долю ко-торых приходится более 50% случаев аутопсий пациентов с деменцией [10–12].”
Qiu, T., Hong, H., Zeng, Q., Xu, X., Wang, Y., Zhu, L., Zhang, L., Li, K., Dai, S., Li, X., et al. (2024) · Journal of Neurology · doi:10.1007/s00415-024-12218-2 · Cited by 2
“In addition to well-established amyloid accumulation, cerebral small vessel disease (SVD) has also been a crucial factor influencing the development of AD [1].”
The Association of Ancillary Diagnostic Tests With Outcome in Dementia
Lindhout, J. E., Richard, E., Hafdi, M., Perry, M., van Charante, E. P. M., & van Gool, W. A. (2024) · Journal of the American Medical Directors Association · doi:10.1016/j.jamda.2024.105040 · Cited by 2
Vascular Risk Factors and Brain Health in Aging: Insights from a Community-Based Cohort Study
Wang, W., Yang, Y., Sang, F., Chen, Y., Li, X., Chen, K., Wang, J., & Zhang, Z. (2024) · Journal of Alzheimer s Disease · doi:10.3233/jad-240240 · Cited by 2
Nonarteritic Anterior Ischemic Optic Neuropathy and the Risk of Dementia
Kim, J., Han, K., Jung, J., Park, K., & Oh, S. Y. (2024) · Neurology · doi:10.1212/wnl.0000000000209657 · Cited by 2
Zheng, W., Lin, D., Shi, S., Ren, J., Wu, J., Wang, M., & Wan, S. (2024) · Journal of Alzheimer s Disease Reports · doi:10.1177/25424823241289804 · Cited by 2
Charisis, S., Mourtzi, N., Scott, M. R., Ntanasi, E., Mamalaki, E., Hatzimanolis, A., Ramı́rez, A., Lambert, J., Yannakoulia, M., Kosmidis, M. H., et al. (2025) · The Journal of Prevention of Alzheimer s Disease · doi:10.1016/j.tjpad.2024.100018 · Cited by 3
Kan, C. N., Hilal, S., Xu, X., et al. (2025) · Acta Neuropsychiatrica · doi:10.1017/neu.2025.8 · Cited by 2
“…involving cerebral microvascular changes, pathogenic factors (e.g. impaired cerebral perfusion, neurovascular regulation, and blood-brain-barrier function), brain volume loss, and further structural cerebral lesions has also been widely discussed (Attems and Jellinger, 2014; Liu et al ., 2015).”
Toraih, E. A., Siddiqui, S., Siddiqui, S., Shirini, K., Elfezzani, N., ABDELMAKSOUD, A., Elshazli, R. M., Hussein, M. H., Elmorsy, E. M., & Fawzy, M. S. (2025) · Neuroepidemiology · doi:10.1159/000545369 · Cited by 2
“While our fi ndings show signi fi cant associations with a range of neurodegenerative conditions, it is important to consider that many of these disorders, such as Alzheimer ’ s disease and vascular dementia, frequently coexist, leading to overlapping clinical symptoms [18].”
Onda, K., Chotiyanonta, J. S., Cowley, H., Uchida, Y., Nowrangi, M. A., Adams, R., Lyketsos, C. G., Zandi, P. P., & Oishi, K. (2025) · International Psychogeriatrics · doi:10.1016/j.inpsyc.2025.100105 · Cited by 2
“Alzheimer's disease (AD) and related dementias (ADRD), including vascular dementia (VaD) and mixed dementia, progressively impair cognitive abilities, leading to disability and loss of independence [1-6].”
Kim, T., Zhang, K., Zhu, T., Song, I., Na, S., Hippe, D. S., Cantón, G., Hatsukami, T. S., Yuan, C., Mossa‐Basha, M., et al. (2025) · Journal of the Neurological Sciences · doi:10.1016/j.jns.2025.123598 · Cited by 2
Giovanna, A. P. D., Tibo, A., Silvestri, L., et al. (2017) · Proceedings of SPIE, the International Society for Optical Engineering/Proceedings of SPIE · doi:10.1117/12.2285044 · Cited by 2
Cerebral Multimorbidity in Aging
Jellinger, K. A. (2016) · Journal of Neurology and Neuromedicine · doi:10.29245/2572.942x/2017/1.1001 · Cited by 2
Self-citationSharafi, S. M., Sylvestre, J., Chevrefils, C., Soucy, J., & Lesage, F. (2019) · Clinical and Translational Neurophotonics · doi:10.1117/12.2508557 · Cited by 2
Cerebrovascular Disease and Hypertension
Sidhu, N. S., & Kaur, S. (2021) · IntechOpen eBooks · doi:10.5772/intechopen.101180 · Cited by 2
Isolation and Functional Analysis of Arteriolar Endothelium of Mouse Brain Parenchyma
Hakim, M. A., Pires, P. W., & Behringer, E. J. (2022) · Journal of Visualized Experiments · doi:10.3791/63463 · Cited by 2
Dib, M., Ampil, E. R., Kee, H. F., Krespi, Y., Mahdawi, A. M. A., Ogun, S. A., Pakdaman, H., & Rejdak, K. (2022) · Journal of Neurology Research Review & Reports · doi:10.47363/jnrrr/2022(4)160 · Cited by 1
Mu, R., Qin, X., Zheng, W., Yang, P., Huang, B., Li, X., Liu, F., Deng, K., & Zhu, X. (2024) · Quantitative Imaging in Medicine and Surgery · doi:10.21037/qims-23-1464 · Cited by 2
“Amide proton transfer (APT) imaging is an MRI technique that reflects the protein and polypeptide content in tissues (10,13).”
BackgroundLipid associated polygenic enrichment in Alzheimer’s diseasePreprint
Broce, I., Tan, C. H., Fan, C. C., Witoelar, A., Wen, N., Jansen, I. E., Hess, C. P., Dillon, W. P., Glastonbury, C. M., Glymour, M. M., et al. (2018) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/383844 · Cited by 2
“Co-occurrence of CV and AD pathology is the most common cause of dementia among the elderly [4] and imaging manifestations of vascular disease are routinely observed on MRI scans of AD patients [36].”
BackgroundFMNL2 interacts with cerebrovascular risk factors to alter Alzheimer’s disease riskPreprint
Raghavan, N. S., Sariya, S., Lee, A., Gao, Y., Reyes‐Dumeyer, D., Jager, P. L. D., Bennett, D. A., Menon, V., Lantigua, R., Kukull, W. A., et al. (2020) · medRxiv · doi:10.1101/2020.08.30.20184879 · Cited by 2
“Neuropathological data indicate that brain tissue from up to 70% of patients with AD have the hallmark neuritic plaques and neurofibrillary tangles with varying degrees of cerebrovascular disease[1-4].”
BackgroundProstacyclin as a Negative Regulator of Angiogenesis in the NeurovasculaturePreprint
Womack, T., Li, J., Govyadinov, P. A., Mayerich, D. M., & Eriksen, J. L. (2021) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2021.04.28.441854 · Cited by 2
“The two most common forms of vascular pathologies in AD are cerebral amyloid angiopathy and small vessel disease [3].”
BackgroundEffect of herpes zoster vaccination on dementia occurrence: A quasi-experimental study in AustraliaPreprint
Pomirchy, M., Bommer, C., Pradella, F., Michalik, F., Peters, R. K., & Geldsetzer, P. (2024) · medRxiv · doi:10.1101/2024.06.27.24309563 · Cited by 2
“…vasculopathy ( 60 , 61 ), amyloid deposition and aggregation of tau proteins ( 62 ), neuroinflammation ( 63 – 66 ), as well as cerebrovascular disease resembling that seen in Alzheimer’s disease, including small to large vessel disease, ischemia, infarction, and hemorrhage ( 67 , 68 , 63 – 66 ).”
Schuldt, B. R., Haworth-Staines, D., Arévalo, A. P., Broekaart, D. W. M., Harlock, A., Wang, L., Bright, A., Gallagher, G., Rabinowitz, G., Goate, A., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.09.04.674192 · Cited by 2
Ali, M. A., Siam, M. H. B., Vardaman, D., Bolding, C., Brazell, J. N., Whatley, A. D., Risley, C. A., Tidwell, H., Hossain, S. N., Samal, J., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2025.12.10.693494 · Cited by 2
Astrocytes and the Synucleinopathies
Koob, A. O., & Sacchetti, P. (2018) · Springer eBooks · doi:10.1007/978-981-13-0944-1_8 · Cited by 1
Marzban, S., Dastgheib, Z. A., Lithgow, B. J., et al. (2024) · Medical & Biological Engineering & Computing · doi:10.1007/s11517-024-03110-2 · Cited by 1
“In addition, recent studies show many patients diagnosed with AD can also have a subtype of AD mixed with cerebrovascular symptomology (AD-CVD) [10].”
Oltra, J., Kalpouzos, G., Ekström, I., Larsson, M., Li, Y., Qiu, C., & Laukka, E. J. (2025) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2025.1539508 · Cited by 1
“…that cerebrovascular co-pathologies are also common in AD and Lewy body diseases [i.e., Parkinson’s disease (PD) and dementia with Lewy bodies] (Attems and Jellinger, 2014; Hijazi et al., 2022), which have a high prevalence of olfactory dysfunctions (Bagherieh et al., 2023; Silva et al., 2018).”
Genius, P., Rodríguez‐Fernández, B., Minguillón, C., Brugulat‐Serrat, A., Huguet, J., Esteller, M., Sudre, C. H., Cortés‐Canteli, M., Tristão‐Pereira, C., García‐Lunar, I., et al. (2026) · Frontiers in Neurology · doi:10.3389/fneur.2025.1667424 · Cited by 1
Tripathi, S. M., Shiells, H., Waymont, J. M. J., Staff, R. T., Schelter, B. O., Bentham, P., Wischik, C. M., & Murray, A. D. (2026) · Current Alzheimer Research · doi:10.2174/0115672050399596251106033110 · Cited by 2
Koychev, I. G., Vaci, N., Moonen, J. E. F., Reid, G., Howgego, G., Yaffe, K. S., Nasrallah, I. M., Sidney, S. S., Jindra, C., Gallacher, J., et al. (2026) · Journal of Alzheimer s Disease · doi:10.1177/13872877251401482 · Cited by 1
“Poor cardiovascular health contributes to dementia both directly, through cerebrovascular pathology causing a degree of vascular dementia 48,49 and impaired regulation of cerebral blood fl ow, 50 and indirectly by accelerating the development of Alzheimer ’ s disease.”
Snorradóttir, Á. Ó., Hafsteinsson, H. K., Hansdottir, K., Ingþórsson, S., Gudmundsson, S. R., Skodras, A., Ísaksson, H. J., & Hakonarson, H. H. (2026) · Acta Neuropathologica Communications · doi:10.1186/s40478-026-02233-x · Cited by 1
Tang, S., Thropp, P., Hausle, I., Younes, K., & Tosun, D. (2026) · Frontiers in Neuroscience · doi:10.3389/fnins.2026.1772024 · Cited by 1
“Alzheimer’s disease (AD) is a multifactorial disorder with etiology that frequently overlaps with other neurodegenerative disorders, such as cerebrovascular disease (CVD; Wardlaw et al., 2020; Scheffer et al., 2021; Attems and Jellinger, 2014), complicating diagnosis and treatment.”
Peripheral biomarkers of neuroinflammation in Alzheimer’s disease and vascular dementia
Ouyang, X., Chia, R. S. L., Chai, Y. L., Chong, Sim, M. A., Jo, D., Arumugam, T. V., Sethi, G., Dawe, G. S., Chen, C. P., et al. (2026) · Biochemical Pharmacology · doi:10.1016/j.bcp.2026.118077 · Cited by 1
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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