Vascular Contributions to Cognitive Impairment and Dementia: A Statement for Healthcare Professionals From the American Heart Association/American Stroke Association

In the paper

“Vascular oxidative stress and inflammation impede the proliferation, migration, and differentiation of oligodendrocyte progenitor cells and compromise repair of the damaged white matter.108,132,133”

What the sources say

• ?Not checked — no full text of the sourcecites [108] source
• Partly supported

  The Discussion (page unavailable) reports that cultured rat OPCs were vulnerable to hydrogen-peroxide oxidative stress, and the paper states that OPCs contribute to white-matter repair. It does not show that vascular oxidative stress or inflammation impedes OPC proliferation, migration, or differentiation, or directly demonstrate impaired repair of damaged white matter. (LLM, conf=0.88)

  cites [132] sourceExperimental — accuracy not yet measured
• Disputed

  The Discussion states that the inflammatory response associated with demyelination provides a powerful impetus for remyelination—the opposite of the claim that inflammation impedes repair. The paper attributes impaired progenitor recruitment and differentiation to aging, but the cited passages do not establish vascular oxidative stress as their cause. No page number is supplied in our copy. (LLM, conf=0.86)

  Checked by a reasoning model — may be wrong.

  cites [133] sourceExperimental — accuracy not yet measured

In the paper

“It is unclear what confounding factors were taken into account in these analyses.322”

What the sources say

• Disputed

  The Methods section explicitly states which factors were included in the adjusted models, including demographics, cardiovascular and dementia risk factors, smoking, physical activity, and ApoE genotype. The claim that it is unclear which confounding factors were taken into account is therefore contrary to the cited paper's account. (LLM, conf=0.89)

  Checked by a reasoning model — may be wrong.

  cites [322] sourceExperimental — accuracy not yet measured

In the paper

“The risk of new-onset dementia after a stroke is approximately twice the rate for age- and sex-matched control subjects270 and averages ≈10% after the first stroke, depending on the location, volume of damaged brain tissue,30 clinical severity, and presence of early poststroke complications (seizure, delirium, hypoxia, hypotension).”

What the sources say

• ?Not checked — no full text of the sourcecites [270] source
• Disputed

  The citation is attached to the claim that new-onset dementia risk is approximately twice that of age- and sex-matched controls. The Results report an adjusted odds ratio of 9.4 for dementia after stroke versus stroke-free controls, and the methods say the groups differed by sex; the study assessed dementia three months after stroke rather than establishing new onset. The later ≈10% and complication claims are not attached to this citation. (LLM, conf=0.90)

  Checked by a reasoning model — may be wrong.

  cites [30] sourceExperimental — accuracy not yet measured

In the paper

“(3) patients at low risk for dementia (young mean age)441,445 and with high baseline MMSE;”

What the sources say

• Disputed

  The Methods (Selection) explicitly exclude pharmaceutical clinical trial volunteers and restrict the review to community-dwelling adults aged 60 or older. The Results (Cognitive Dysfunction) describe population-based prospective studies with mean baseline ages including 68.9, 75.6, and 83 years, rather than trials characterized by a young mean age. The paper mentions MMSE as an outcome measure but does not establish that participants had high baseline MMSE scores. (LLM, conf=0.82)

  Checked by a reasoning model — may be wrong.

  cites [441] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [445] source

In the paper

“Executive dysfunction has not been shown to specifically point to cerebrovascular disease, whereas a pattern of memory deficits may be associated more with Alzheimer disease and its associated pathology than with cerebrovascular disease.”

What the sources say

• ?Not checked — no full text of the sourcecites [49] source
• Supported

  The Discussion (page not specified) says severe memory impairment strongly points to Alzheimer-type brain pathology, while executive deficits are a much weaker diagnostic marker of vascular disease. It relates this finding in MCI patients to reported results in patients with autopsy-defined Alzheimer and vascular pathology. (LLM, conf=0.91)

  cites [50] source

In the paper

“Chronic macroscopic infarcts are very common, occurring in approximately one third to one half of older people,13,54–56 a frequency far greater than the frequency of clinical stroke.”

What the sources say

• ?Not checked — no full text of the sourcecites [13] source
• Partly supported

  The Results (Probable AD in the community versus clinic; page unavailable) report that macroscopic infarcts were more common in the community cohort than in the clinic cohort. The available passages do not establish that they occurred in one third to one half of older people or that their frequency was far greater than that of clinical stroke. (LLM, conf=0.81)

  cites [54] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [55] source
• ?Not checked — no full text of the sourcecites [56] source

In the paper

“There are other common vascular pathologies in the brains of older people, including white matter degeneration70,71 and primary vessel disease (ie, arteriolosclerosis/lipohyalinosis, atherosclerosis, and cerebral amyloid angiopathy [CAA]).70,72,73”

What the sources say

• ?Not checked — no full text of the sourcecites [70] source
• ?Not checked — no full text of the sourcecites [71] source
• ?Not checked — no full text of the sourcecites [72] source
• Partly supported

  The Discussion (page not available) says sclerotic medullary arteries are commonly seen in older people and that some are associated with diffuse ischemic white matter change. The Results (page not available) describe fibrohyaline thickening but state that atherosclerosis and amyloid angiopathy were not observed in the medullary arteries. This paper therefore supports part of the broad claim, not the full list of vessel diseases as common findings in its studied arteries. (LLM, conf=0.88)

  cites [73] sourceExperimental — accuracy not yet measured

In the paper

“Although the specific importance of subcortical infarcts and interaction has not been confirmed, subsequent studies have established that infarcts are additive with Alzheimer disease pathology in lowering cognitive function17,57 and increasing the odds of dementia17,18,62,63 or clinical Alzheimer disease.61”

What the sources say

• ?Not checked — no full text of the sourcecites [17] source
• ?Not checked — no full text of the sourcecites [57] source
• ?Not checked — no full text of the sourcecites [18] source
• Partly supported

  Split into 2 atoms — 1 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 1 unverifiable. Expand the claim to see per-atom verdicts.

  cites [62] sourceExperimental — accuracy not yet measured
• Partly supported

  Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  cites [63] sourceExperimental — accuracy not yet measured
• Partly supported

  Split into 2 atoms — 1 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 1 unverifiable. Expand the claim to see per-atom verdicts.

  cites [61] sourceExperimental — accuracy not yet measured

In the paper

“In addition, most people with dementia12 and almost half of those with clinically probable Alzheimer disease61 have mixed pathology, most commonly Alzheimer disease and infarcts.”

What the sources say

• ?Not checked — no full text of the sourcecites [12] source
• Supported

  The Results section on probable Alzheimer disease reports mixed pathologies in 45.8% of people with clinically probable AD and identifies AD with infarcts as the most common combination. The separate claim about most people with dementia is attached to citation 12, not this source. (LLM, conf=0.94)

  cites [61] source

In the paper

“In animal models, the major risk factors for VCI and Alzheimer disease —hypertension, aging, and diabetes110—impair endothelium-dependent responses in the cerebral microcirculation and blunt functional hyper-emia.101,111,112”

What the sources say

• ?Not checked — no full text of the sourcecites [110] source
• ?Not checked — no full text of the sourcecites [101] source
• Partly supported

  The Discussion (page unavailable) reports that aging impairs endothelial function in mouse cerebral arteries and states that neurovascular coupling decreases with aging. The study tested isolated basilar arteries, not functional hyperemia, and the cited passages do not establish the claimed effects of hypertension or diabetes. (LLM, conf=0.88)

  cites [111] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [112] source

In the paper

“These endothelial mediators subserve functions as varied as local flow distribution,91 immune surveillance (in concert with perivascular cells),92 and hemostatic balance.93”

What the sources say

• ?Not checked — no full text of the sourcecites [91] source
• Supported

  Citation 92 is attached to immune surveillance in concert with perivascular cells, not to local flow distribution or hemostatic balance. The Discussion (‘What are perivascular cells?’; page unavailable) explicitly says perivascular cells participate in nervous-system immune surveillance, while the Introduction describes their interaction with endothelial cells in responses to immune signals. (LLM, conf=0.88)

  cites [92] source
• ?Not checked — no full text of the sourcecites [93] source

In the paper

“Cerebral smooth muscle cells of patients with Alzheimer disease have increased constrictor tone,118 which may contribute to the CBF reduction observed in this condition.100”

What the sources say

• Supported

  The Discussion reports that vascular smooth muscle cells from the cerebral vessels of patients with Alzheimer disease had a hypercontractile phenotype. It also suggests this phenotype could contribute to brain hypoperfusion, although the citing sentence attaches this source specifically to the increased-constrictor-tone clause. (LLM, conf=0.93)

  cites [118] source
• ?Not checked — no full text of the sourcecites [100] source

In the paper

“Microvessels have thickened basement membranes, become tortuous, and are reduced in number.71,105–107”

What the sources say

• ?Not checked — no full text of the sourcecites [71] source
• ?Not checked — no full text of the sourcecites [105] source
• Partly supported

  The Introduction describes tortuosity in arterioles supplying the deep white matter in leukoaraiosis, while the Abstract reports reduced microvascular density in leukoaraiosis and preliminary evidence of reduced density in Alzheimer’s disease. Neither passage describes thickened basement membranes, and the tortuosity finding is not established for Alzheimer’s disease. Page numbers are unavailable in our copy. (LLM, conf=0.88)

  cites [106] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [107] source

In the paper

“The brain depends on a continuous blood supply, and interruption of cerebral blood flow (CBF) leads to brain dysfunction and death.86”

What the sources say

• Supported

  The “Parenchymal Failure” section says the brain is especially vulnerable to ischemia: neurological dysfunction occurs within seconds to minutes of vessel occlusion, while injury and cell death develop over time. Its discussion of salvageable tissue also explains that tissue with impaired perfusion dies unless perfusion improves or cells are protected. (LLM, conf=0.93)

  cites [86] source

In the paper

“Endothelial cells exert trophic actions that are critical in brain development, neuroplasticity, and repair when endothelial growth factors orchestrate the migration and differentiation of neuroblasts.96–99”

What the sources say

• ?Not checked — no full text of the sourcecites [96] source
• Partly supported

  The Discussion reports that endothelial cells secrete factors regulating neuronal differentiation in vitro and that vascular ligands guide neuroblast migration after stroke. It does not establish that those ligands orchestrate neuroblast differentiation, or that these actions are critical across brain development and neuroplasticity. The relevant indexed passages have no page numbers. (LLM, conf=0.86)

  cites [97] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [98] source
• ?Not checked — no full text of the sourcecites [99] source

In the paper

“the low-density lipoprotein receptor–related protein-1, a critical Aβ brain clearance receptor, is downregulated in cerebral blood vessels of patients with Alzheimer disease, leading to accumulation of amyloid around blood vessels and worsening of vascular dysfunction.129”

What the sources say

• Partly supported

  Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  cites [129] sourceExperimental — accuracy not yet measured

In the paper

“Pittsburgh Compound B retention is not specific for CAA as opposed to Alzheimer disease, because the compound binds to both vascular and parenchymal amyloid158; however, the 2 pathologies may be distinguishable in part by the relative occipital predominance of labeling in CAA.156,157”

What the sources say

• Partly supported

  Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  cites [158] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [156] source
• ?Not checked — no full text of the sourcecites [157] source

In the paper

“a single nucleotide polymorphism in the COL4A1 gene was associated with pulse wave velocity, an index of arterial stiffness, in a population.180”

What the sources say

• Supported

  The Abstract Background identifies pulse wave velocity (PWV) as an index of central arterial stiffness. The Abstract Methods and Results reports that the COL4A1 SNP rs3742207 was associated with PWV in the Sardinian cohort and that the association was replicated in an Old Order Amish population. (LLM, conf=0.95)

  cites [180] source

In the paper

“The presence of multiple strictly lobar hemorrhages in the absence of other definite causes such as head trauma, brain tumor, or supratherapeutic anticoagulation has been defined by the Boston criteria as “probable CAA” and validated against neuropathologically or genetically diagnosed CAA.153,154”

What the sources say

• ?Not checked — no full text of the sourcecites [153] source
• Partly supported

  Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  cites [154] sourceExperimental — accuracy not yet measured

In the paper

“The lumen-intima and media-adventitia separation can be determined to within ≈0.1 mm on longitudinal B-mode ultrasound images of the extracranial carotid arteries where these interfaces are readily apparent.183,184”

What the sources say

• ?Not checked — no full text of the sourcecites [183] source
• Partly supported

  The Subjects and Methods section (page not specified in our copy) describes measurements of the far-wall intimal-medial thickness in extracranial carotid arteries and reports approximately 0.10 mm axial resolution. That is the minimum spacing at which adjacent boundaries can be distinguished, not a demonstrated measurement accuracy of within 0.1 mm; the paper also does not specify longitudinal images for this claim. (LLM, conf=0.82)

  cites [184] sourceExperimental — accuracy not yet measured

In the paper

“Mutations of the COL4A1 type IV collagen subunit gene have also been reported in association with congenital porencephaly, leukoencephalopathy, or intracerebral hemorrhage.178,179”

What the sources say

• Supported

  The paper’s Results and Conclusions report COL4A1 mutations in families with porencephaly and identify a predisposition to perinatal cerebral haemorrhage. The Affected section also describes white-matter lesions in mutation carriers, supporting the leukoencephalopathy part of the paraphrase. Passage-level page numbers are not available in our copy. (LLM, conf=0.88)

  cites [178] source
• ?Not checked — no full text of the sourcecites [179] source

In the paper

“Other potential diagnostic approaches have been explored, including detection of reduced Aβ in cerebrospinal fluid155 or increased retention of the amyloid ligand Pittsburgh Compound B on positron emission tomography imaging.156,157”

What the sources say

• Supported

  The Discussion reports decreased CSF Aβ40 and Aβ42 in patients with cerebral amyloid angiopathy and says CSF analysis may help identify them. This supports the potential CSF diagnostic approach attributed to this source; the PET approach has separate citations. (LLM, conf=0.94)

  cites [155] source
• ?Not checked — no full text of the sourcecites [156] source
• ?Not checked — no full text of the sourcecites [157] source

In the paper

“Although no treatments have been identified to modify the course of CADASIL, it is notable that cardiovascular risk factors such as hypertension, elevated hemoglobin A1c, and smoking may be associated with a worse clinical and radiographic phenotype.171,172”

What the sources say

• ?Not checked — no full text of the sourcecites [171] source
• Partly supported

  The Results (Presence of CM and associated factors; Cerebral microhaemorrhages and neurological outcome, pages unavailable) associate hypertension and elevated HbA1c with microhaemorrhages, and systolic blood pressure with poor functional outcome. The Discussion says treatment benefits remain to be tested. But the study does not support including smoking: its tables show no significant association with either microhaemorrhages or poor functional outcome. (LLM, conf=0.90)

  cites [172] sourceExperimental — accuracy not yet measured

In the paper

“Several pathways may link aortic stiffness to microvascular brain damage. They include endothelial dysfunction and oxidative stress,209 a mutually reinforcing remodeling of large and small vessels (ie, large-/small-artery cross talk),210 and exposure of small vessels to the high-pressure fluctuations of the cerebral circulation,211”

What the sources say

• ?Not checked — no full text of the sourcecites [209] source
• ?Not checked — no full text of the sourcecites [210] source
• Supported

  Citation 211 is attached to the claim that small cerebral vessels are exposed to high-pressure fluctuations, not to the preceding pathways. The Abstract (p. 200) says that high flow and low resistance expose small vessels to pressure fluctuations in the carotid and vertebral arteries, providing a proposed explanation for microvascular damage. (LLM, conf=0.94)

  cites [211] source

In the paper

“Retinal arterial narrowing correlates with increased arterial stiffness219 and cerebral small-vessel disease.218,220,221”

What the sources say

• Supported

  Citation 219 supports the arterial-stiffness portion of the sentence; the cerebral small-vessel disease portion has separate citations. The Discussion (page not supplied) reports an association between aortic stiffening and retinal arteriolar narrowing in participants free of clinical cardiovascular disease. (LLM, conf=0.94)

  cites [219] source
• ?Not checked — no full text of the sourcecites [218] source
• ?Not checked — no full text of the sourcecites [220] source

In the paper

“The well-known, age-related arterial stiffening process (arteriosclerosis) is associated with quantitatively less elastin and more collagen but is also associated with qualitative changes in the arterial wall.143,199,200”

What the sources say

• ?Not checked — no full text of the sourcecites [143] source
• Partly supported

  In “Determinants of Arterial Stiffness” (page not available), the paper links aging to thinning and fragmentation of elastic fibers, increased collagenous material, and qualitative changes in the arterial wall. It does not explicitly establish a quantitative decrease in elastin, so that part of the claim is not fully supported. (LLM, conf=0.83)

  cites [199] sourceExperimental — accuracy not yet measured
• Partly supported

  The Essential Hypertension section (page unavailable) says central arteries stiffen with age, elastic fibers lose their orderly arrangement and undergo thinning and fragmentation, and collagenous material increases. These passages support age-related stiffening, increased collagen, and qualitative wall changes, but they do not establish a quantitative decrease in elastin content. (LLM, conf=0.84)

  cites [200] sourceExperimental — accuracy not yet measured

In the paper

“This relationship was significant after controlling for age and education; some studies further adjusted for the presence of depressive symptoms187,189 and/or cardiovascular risk factor level.189”

What the sources say

• ?Not checked — no full text of the sourcecites [187] source
• Supported

  The Abstract’s Methods section says the analyses adjusted for age, education, depressive symptoms, and cardiovascular risk factors including mean arterial pressure, body mass index, total cholesterol, and smoking. The Abstract’s Results section reports accelerated cognitive decline among participants with greater carotid IMT after those adjustments. The supplied passages do not give page numbers. (LLM, conf=0.93)

  cites [189] source

In the paper

“The mechanisms by which atherosclerotic cerebrovascular pathology might be associated with VCI include thrombotic occlusion of large vessels with subsequent chronic cerebral hypoperfusion; cerebral embolism originating from ruptured or thrombotic carotid plaques and targeting distal vessels; increased parenchymal oxidative stress; blood pressure dys-regulation affecting BBB integrity; and a common”

What the sources say

• Partly supported

  The Discussion proposes chronic cerebral hypoperfusion as a mechanism linking subclinical vascular disease to cognitive impairment. It does not specify thrombotic large-vessel occlusion as its cause, or describe plaque-derived embolism, parenchymal oxidative stress, or blood-pressure dysregulation affecting blood–brain barrier integrity. No page number is available in our copy. (LLM, conf=0.88)

  cites [189] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [195] source
• Partly supported

  The Discussion (page not provided) proposes chronic cerebral hypoperfusion as a contributor to brain dysfunction in patients with cardiovascular disease. The Abstract (page not provided) also links atherosclerosis to cerebral vessel changes and blood-pressure abnormalities to impaired cerebral hemodynamics. Our copy does not support the specified mechanisms of large-vessel thrombotic occlusion, carotid-plaque embolism, oxidative stress, or blood-pressure effects on blood–brain barrier integrity. (LLM, conf=0.88)

  cites [196] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [197] source
• Partly supported

  The “Carotid Disease and the Brain” section (page unavailable) proposes large-vessel occlusion with hypoperfusion and embolism from ruptured or thrombotic carotid plaques. It does not describe the hypoperfusion as chronic or propose oxidative stress or blood-pressure dysregulation affecting blood–brain barrier integrity as mechanisms. (LLM, conf=0.90)

  cites [198] sourceExperimental — accuracy not yet measured

In the paper

“Importantly, age-specific definitions of extensive WMLs can be created240 and prove useful in defining risk for VCI in a community cohort.240”

What the sources say

• Partly supported

  The Methods (MRI scans; page not provided) define extensive white matter hyperintensity volume using age-specific thresholds. The Results and Discussion report that this measure predicted incident dementia in a community cohort and amnestic MCI only among participants aged 60 or older. The study did not specifically establish risk for vascular cognitive impairment (VCI). (LLM, conf=0.86)

  cites [240] sourceExperimental — accuracy not yet measured

In the paper

“Similarly, WMLs have been associated with declining scores in the modified MMSE and the Digit Symbol Substitution Test,246,247 as well as with incident MCI, dementia, and death.240”

What the sources say

• Partly supported

  The Results sections on dementia, MCI, and mortality associate white matter hyperintensity measures with incident dementia and death. For MCI, however, the paper finds no overall association; increased risk of amnestic MCI appears only in certain subgroups, including participants aged 60 or older. The unqualified reference to incident MCI overstates that finding. (LLM, conf=0.88)

  cites [240] sourceExperimental — accuracy not yet measured

In the paper

“Estimates of the prevalence of silent cerebral infarction on MRI in community-based samples vary between 5.8% and 17.7%, with an average of 11%, depending on age, ethnicity, presence of comorbidities, and imaging techniques.237”

What the sources say

• Partly supported

  The Abstract’s Background and Purpose gives the 5.8%–17.7% range for community-based MRI samples and attributes variation to age, ethnicity, comorbidities, and imaging techniques. It does not give an 11% average across those samples; the Abstract’s Results report 10.7% for the Framingham sample alone. (LLM, conf=0.86)

  cites [237] sourceExperimental — accuracy not yet measured

In the paper

“Interestingly, although most studies suggest that these measures of CVBI are usually associated with non–memory-related cognitive deficits,241 a number of studies also show similar associations with memory impairment.240,242,243”

What the sources say

• ?Not checked — no full text of the sourcecites [241] source
• Supported

  The citation is attached to the sentence’s memory-impairment claim, not its statement about non-memory deficits. In Results (page not provided), the paper reports that white matter hyperintensity measures were associated with incident amnestic mild cognitive impairment among participants aged 60 or older, providing an example of the claimed association. (LLM, conf=0.91)

  cites [240] source
• ?Not checked — no full text of the sourcecites [242] source

In the paper

“Most have a single lesion, and the infarcts are most often located in the basal ganglia (52%), followed by other subcortical (35%) and cortical (11%) areas.237”

What the sources say

• Supported

  The Abstract’s Results report that 84% of participants with silent cerebral infarcts had a single lesion. They give the same location breakdown: 52% basal ganglia, 35% other subcortical areas, and 11% cortical areas. (LLM, conf=0.95)

  cites [237] source

In the paper

“In the Framingham study, for example, the prevalence of silent cerebral infarction between the fifth and seventh decades of life is ≈10% but increases rapidly in the eighth decade to 17% and in the ninth decade to nearly 30%.”

What the sources say

• Partly supported

  The Results report 10.7% prevalence overall in the Framingham Offspring sample and an increase with age, from under 8% at ages 30–49 to over 15% at ages 70–89. Our copy does not give the claimed decade-specific figures of 17% in the eighth decade or nearly 30% in the ninth; the Results refer to Figure 1 for age-specific data without stating those values in the retrieved text. (LLM, conf=0.83)

  cites [237] sourceExperimental — accuracy not yet measured

In the paper

“Gray matter volumes, however, were associated with both vascular and Alzheimer disease processes, and hippocampal volumes were associated with both hippocampal sclerosis and Alzheimer disease.”

What the sources say

• Supported

  The Results section (‘Associations between Magnetic Resonance Hippocampal Volume and Pathology’) reports that Alzheimer disease pathology and hippocampal sclerosis were both inverse correlates of hippocampal volume and jointly accounted for 33% of its variance. The Discussion also states that hippocampal volume is related to both processes. (LLM, conf=0.95)

  cites [82] source

In the paper

“For example, the presence of SBI more than doubles the risk of dementia and risk of stroke.240,244,245”

What the sources say

• Partly supported

  The indexed Results summary reports that MRI-defined brain infarcts (BI) were associated with more than double the risk of incident stroke (HR 2.84) and dementia (HR 6.12). However, the Methods define BI by MRI appearance, not by whether the infarct was silent; the Results also include participants with prior stroke. The reported estimates therefore do not specifically establish the claim for silent brain infarcts (SBI). (LLM, conf=0.83)

  cites [240] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [244] source
• ?Not checked — no full text of the sourcecites [245] source

In the paper

“In a study that examined the pathological correlates of in vivo MRI evidence of CVBI,82 WMLs were highly correlated with pathological features of ischemic white matter injury but not Alzheimer disease pathology.”

What the sources say

• Supported

  The Discussion reports that white matter hyperintensities (WMH) were associated with vascular disease and complete or incomplete infarction, but not with AD pathology. The Results add that white matter pathology and age explained 32% of WMH variance in the final multivariate model. An unadjusted analysis did find a correlation with AD pathology, so the ‘not with AD’ finding refers to the paper’s adjusted interpretation. (LLM, conf=0.90)

  cites [82] source

In the paper

“The cognitive tests for VCI are, to a degree, nonspecific for vascular disease, and different criteria for VaD identify different sets of people.29”

What the sources say

• Supported

  The Discussion (page not available in our copy) reports that executive-function scores did not differ between VaD and non-VaD subgroups and that AD can contribute to the executive deficits seen in VaD, supporting the qualified point that cognitive tests are not specific to vascular disease. It also says different VaD criteria missed different MRI-confirmed cases; the Criteria agreement section reports disagreement among the criteria. (LLM, conf=0.88)

  cites [29] source

In the paper

“Recent studies have shown that similar to Western countries, Alzheimer disease is the leading cause of dementia in Asian populations.275”

What the sources say

• Partly supported

  The Results (p. 3) report that Alzheimer’s disease accounted for most dementia cases in this US cohort, supporting the Western comparison. The paper does not report whether it is the leading cause of dementia in Asian populations, which is the claim’s central point. (LLM, conf=0.82)

  cites [275] sourceExperimental — accuracy not yet measured

In the paper

“In a pooled analysis of major European population–based studies, VaD was prevalent in 1.6% of subjects >65 years of age, but there was a large variation in 5-year age-specific prevalence.264”

What the sources say

• ?Could not verify

  The Results and Statistical analysis sections describe a Boston dietary-questionnaire validation sample, not a pooled analysis of European population-based studies. Searches for vascular dementia, 1.6% prevalence, and five-year age-specific prevalence found no passage addressing the claim. (LLM, conf=0.76)

  cites [264] sourceExperimental — accuracy not yet measured

In the paper

“Recently, 1 study found an association of lower circulating vitamin D levels with poorer cognitive function,294 but another found no association.295”

What the sources say

• ?Not checked — no full text of the sourcecites [294] source
• Supported

  The Discussion reports that low circulating 25(OH)D was associated with impaired cognitive function in elders receiving home health services. The Results also report significant associations with several tests of executive function and attention. The separate finding of no association is attributed to citation 295, not this paper. (LLM, conf=0.94)

  cites [295] source

In the paper

“This age-related increase in VaD follows the pattern of stroke,269 although dementia after stroke may be more frequent in people <80 years old.270”

What the sources say

• Partly supported

  The Results report that all-cause dementia incidence increased with age among people aged 90 and older, and that 22% of examiner-diagnosed cases were vascular dementia. They do not report age-specific vascular dementia rates or compare their pattern with stroke. The separate claim about dementia after stroke in people under 80 is attached to citation 270, not this source. (LLM, conf=0.82)

  cites [269] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [270] source

In the paper

“A recent study reporting on the prevalence of VaD in developing countries reported a range of 0.6% to 2.1%.3,33”

What the sources say

• Supported

  The Vascular dementia section directly reports a VaD prevalence range of 0.6% to 2.1% in developing countries. It specifies that the estimates are for people aged over 65; the citing sentence omits that age qualifier. No page number is provided in our copy. (LLM, conf=0.94)

  cites [3] source
• ?Not checked — no full text of the sourcecites [33] source

In the paper

“Chronic hyperglycemia, increased insulin, the metabolic syndrome, and diabetes are associated with VCI,337,345–348 as well as VaD or dementia with stroke.349,350”

What the sources say

• ?Not checked — no full text of the sourcecites [337] source
• ?Not checked — no full text of the sourcecites [345] source
• ?Not checked — no full text of the sourcecites [346] source
• Partly supported

  The Comment and Results (pages unavailable) link metabolic syndrome and high fasting glucose to cognitive impairment in older women. They do not establish an association specifically with vascular cognitive impairment (VCI), and the paper does not report an association for increased insulin. The citing sentence assigns its separate claim about vascular dementia or dementia with stroke to other citations. (LLM, conf=0.85)

  cites [347] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [348] source
• Supported

  The citation to this paper is attached to the VaD or dementia-with-stroke part of the sentence, rather than the preceding VCI claim. The Discussion (page not specified) states that type 2 diabetes is associated with an increased risk of vascular dementia and discusses Alzheimer's disease with cerebrovascular disease. (LLM, conf=0.90)

  cites [349] source

In the paper

“Body mass index measured in midlife is more strongly associated with VCI, whereas body weight measured later in life has an inverse association with cognitive impairment, where obesity is associated with a lower risk of dementia.320”

What the sources say

• Partly supported

  The Introduction says high BMI has been associated with dementia, and the Results report that women overweight or obese in midlife had a higher blood–brain barrier permeability measure 24 years later. The paper does not establish a stronger association specifically with vascular cognitive impairment (VCI), compare midlife BMI with later-life weight as predictors of cognitive impairment, or report that later-life obesity lowers dementia risk. The cited passages have no page numbers in our copy. (LLM, conf=0.83)

  cites [320] sourceExperimental — accuracy not yet measured

In the paper

“Physical activity may increase brain neurotrophins, such as brain-derived neurotrophic factor, improve cerebrovascular functioning and brain perfusion, reduce response to stress, and increase brain plasticity through synaptogenesis and neurogenesis.302”

What the sources say

• ?Could not verify

  Split into 2 atoms — 0 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 2 unverifiable. Expand the claim to see per-atom verdicts.

  cites [302] sourceExperimental — accuracy not yet measured

In the paper

“A recent review identified older age, lower education, prestroke cognitive impairment, diabetes, and atrial fibrillation as factors that increased the risk, but one of the strongest predictors of cognitive decline after an initial stroke was the occurrence of a second stroke.269,270”

What the sources say

• Partly supported

  Split into 2 atoms — 0 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 1 unverifiable. Expand the claim to see per-atom verdicts.

  cites [269] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [270] source

In the paper

“Specifically, reduced cardiac output has been associated with executive dysfunction (mainly sequencing and planning difficulties)381 and regional WMLs adjacent to the subcortical nuclei.382”

What the sources say

• ?Could not verify

  The Discussion mentions white matter lesions in relation to diabetes, but does not link them to cardiac output or locate them adjacent to subcortical nuclei. Searches for reduced cardiac output and regional white matter lesions found no passage addressing that association. Citation 382 is attached to the white-matter-lesion part of the citing sentence. (LLM, conf=0.76)

  cites [381] sourceExperimental — accuracy not yet measured
• Partly supported

  The Discussion reports that, among older adults with cardiovascular disease, reduced cardiac output was associated with executive dysfunction and white matter hyperintensities. It does not specify sequencing or planning difficulties, or locate the lesions adjacent to subcortical nuclei. The paper’s own Results found only a borderline association with a combined executive-function/information-processing score. (LLM, conf=0.86)

  cites [382] sourceExperimental — accuracy not yet measured

In the paper

“Management of vascular risks and symptomatic pharmacotherapy targeting VaD has been the primary approach.390”

What the sources say

• Supported

  The Primary and Secondary Prevention section describes treatment of vascular risk factors, while Pharmacotherapy in VaD reviews drugs studied for symptomatic treatment. The Conclusions bring these approaches together, emphasizing vascular-risk control and trials of symptomatic agents; the paper also cautions that no symptomatic VaD treatment was officially approved. (LLM, conf=0.86)

  cites [390] source

In the paper

“The importance of balanced nutrition in early life for normal neurocognitive development, a process that is not finished until late adolescence, has been widely recognized.427”

What the sources say

• Partly supported

  The Medical and Public Health Implications section links maternal nutrition and early development with the infant’s cognitive development, supporting the importance of early-life nutrition. It does not say that neurocognitive development continues until late adolescence; no page number is available in our copy. (LLM, conf=0.81)

  cites [427] sourceExperimental — accuracy not yet measured

In the paper

“Cognitive rehabilitation and cognitive stimulation so far have not proven effective.419,420”

What the sources say

• ?Could not verify

  The Methods and Results sections describe trials comparing vinpocetine with placebo, and the Discussion concludes that evidence for vinpocetine's benefit is inconclusive. Searches for cognitive rehabilitation, cognitive stimulation, and nonpharmacological interventions found no passage assessing whether either approach has proven effective. Page numbers were not available in our copy. (LLM, conf=0.76)

  cites [419] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [420] source

In the paper

“Cognitive benefit was found, but global and functional efficacy was less consistent in the individual studies.396,400”

What the sources say

• ?Could not verify

  The Discussion (page unavailable) examines white matter hyperintensities and cognition, and says their effect on response to cholinesterase inhibitors remains to be determined. Searches for donepezil and for global and functional treatment outcomes found no passage assessing those outcomes in vascular dementia. (LLM, conf=0.75)

  cites [396] sourceExperimental — accuracy not yet measured
• Supported

  The Discussion reports a small but significant cognitive improvement in this trial, no difference on the global CIBIC-Plus measure, and consistency with two prior donepezil VaD trials. It also describes a variable effect on activities of daily living, supporting the claim that functional efficacy was less consistent. (LLM, conf=0.92)

  cites [400] source

In the paper

“Results of studies on blood pressure measured in late life and dementia are less consistent, with most finding no association with hypertension or an association with low blood pressure and dementia.343,428”

What the sources say

• ?Not checked — no full text of the sourcecites [343] source
• ?Could not verify

  The Common cause hypothesis and Reverse causality sections discuss cognitive ageing and illness in older people, but neither addresses blood pressure and dementia. Searches for late-life blood pressure, hypertension, and dementia found no passage reporting the claimed pattern of study results. (LLM, conf=0.74)

  cites [428] sourceExperimental — accuracy not yet measured

In the paper

“The treatment was found to have no effect on the risk of dementia or cognitive decline.444”

What the sources say

• Partly supported

  The Introduction (page unavailable) says HYVET-COG confirmed a non-significant reduction in dementia risk, which supports a finding of no statistically significant effect—not proof of no effect. It does not report HYVET-COG's cognitive-decline result; the no-difference finding for cognitive decline in the Discussion concerns PRoFESS patients instead. (LLM, conf=0.86)

  cites [444] sourceExperimental — accuracy not yet measured

In the paper

“In 3 studies there was no association between hypertension treatment and risk of Alzheimer disease,432–434 whereas in others there was a decreased risk of Alzheimer disease among those receiving antihypertensive treatment.429,431,435–437”

What the sources say

• ?Not checked — no full text of the sourcecites [432] source
• Supported

  The citation supports the decreased-risk part of the sentence, not the finding attributed to the three other studies. In the Results (Table 2), participants treated for more than 12 years had lower Alzheimer disease risk than never-treated hypertensive participants; the shorter-treatment groups did not show a clear reduction. Page numbers were not provided in the passages. (LLM, conf=0.91)

  cites [433] source
• ?Not checked — no full text of the sourcecites [434] source
• ?Not checked — no full text of the sourcecites [429] source
• ?Not checked — no full text of the sourcecites [431] source

In the paper

“It was concluded that cognitive dysfunction is an independent predictor of clinical outcomes in patients with type 2 diabetes mellitus but does not modify the effects of blood pressure lowering or glucose control on the risk of major cardiovascular events.458”

What the sources say

• ?Could not verify

  The Background lists diabetes as a possible baseline risk factor, but the Discussion addresses whether blood-pressure lowering prevents cognitive decline or dementia in hypertensive patients without prior cerebrovascular disease. Searches for the claimed independent prediction and for glucose control and major cardiovascular events found no passage addressing those findings in patients with type 2 diabetes. (LLM, conf=0.76)

  cites [458] sourceExperimental — accuracy not yet measured

In the paper

“Treatment with statin therapy has been documented to protect against stroke, both in primary460 and secondary studies, based on data from meta-analysis36 and a single trial, Stroke Prevention by Aggressive Reduction in Cholesterol Levels (SPARCL).461”

What the sources say

• ?Not checked — no full text of the sourcecites [460] source
• ?Not checked — no full text of the sourcecites [36] source
• ?Could not verify

  The Introduction (p. 2) describes ADVANCE as studying blood-pressure lowering and intensive glucose control, and the Discussion (p. 7) discusses stroke in relation to blood-pressure treatment. Searches for statins, SPARCL, and meta-analysis found no passage in our copy addressing the claimed protection against stroke in primary or secondary studies. (LLM, conf=0.76)

  cites [461] sourceExperimental — accuracy not yet measured

In the paper

“A few observational studies have documented that people who consume a Mediterranean diet have better cognition and less risk of dementia than people consuming other diets.470”

What the sources say

• ?Could not verify

  The Introduction (page unavailable) discusses observational findings about NSAID use and Alzheimer’s risk, not Mediterranean diets. Searches for “Mediterranean diet” and “diet cognition dementia risk” found no passage in our copy addressing diet, cognition, or a dietary comparison. (LLM, conf=0.76)

  cites [470] sourceExperimental — accuracy not yet measured

In the paper

“These studies had variable methods in relation to model type (fixed or random) and selection of patients.453,454”

What the sources say

• ?Could not verify

  The Subjects and Methods section describes statistical analyses of the Syst-Eur trial, not a comparison of meta-analyses. Searches for fixed versus random models, patient selection, and meta-analysis found no passage in our copy addressing the claimed variation in methods. Page numbers were not available in the indexed passages. (LLM, conf=0.76)

  cites [453] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [454] source

In the paper

“For example, in a cohort in Finland, the combination of elevated systolic blood pressure, hypercholesterolemia, and obesity increased the risk of Alzheimer disease by ≈6 times, whereas individually, any of these factors alone increased risk by ≈2 times.494”

What the sources say

• ?Could not verify

  Subjects and Methods (p. 2) describes a Finnish cohort of patients with ischemic stroke, while the Discussion (p. 4) compares criteria for diagnosing vascular dementia. Our copy does not address Alzheimer disease risk from the specified combination of blood pressure, cholesterol, and obesity, or report the claimed sixfold and twofold increases (searched those factors and risk estimates). (LLM, conf=0.78)

  cites [494] sourceExperimental — accuracy not yet measured

In the paper

“Carotid intimal-medial thickness and arterial stiffness are emerging as markers of arterial aging and may serve as risk markers for VCI.”

In the paper

“The neuropathology of cognitive impairment in later life is often a mixture of Alzheimer disease and microvascular brain damage, which may overlap and synergize to heighten the risk of cognitive impairment.”

In the paper

“Dementia criteria based on memory deficits are derived from concepts proposed for Alzheimer disease, but these may not be suitable for the dementia syndrome associated with cerebrovascular disease, in which memory-related structures (eg, mesial temporal lobe, thalamus) could be intact, resulting in relatively preserved memory functions.”

What the sources say

• ?Not checked — no full text of the sourcecites [27] source
• ?Not checked — no full text of the sourcecites [28] source

In the paper

“Vascular contributions to cognitive impairment and dementia of later life are common.”

In the paper

“These risks may include but are not limited to atrial fibrillation, hypertension, diabetes mellitus, and hypercholesterolemia.”

In the paper

“As the threshold is expanded, the frequency rates increase accordingly.”

In the paper

“This synergistic effect between Alzheimer disease and cerebrovascular disease pathology may explain why patients with mesial temporal lobe atrophy, presumably attributable to Alzheimer disease, have an increased risk of dementia after stroke compared with those without atrophy, because hippocampal atrophy may also be caused by vascular disease.”

What the sources say

• ?Not checked — no full text of the sourcecites [38] source
• ?Not checked — no full text of the sourcecites [39] source

In the paper

“All of the major criteria for VaD have a different definition of dementia, and this results in challenges in reliability studies.”

What the sources say

• ?Not checked — no full text of the sourcecites [26] source

In the paper

“Furthermore, these same vascular risk factors may be risk markers for Alzheimer disease.”

In the paper

“Although some authors propose that the symptoms should appear within 3 months after a stroke,30 this is arbitrary, and symptoms may develop after this time frame.”

In the paper

“Currently, no specific treatments for VCI have been approved by the US Food and Drug Administration.”

In the paper

“Some studies contend that mixed pathologies, including the degenerative components caused by Alzheimer disease and vascular factors, are the most common explanation for cognitive impairment in aging.”

What the sources say

• ?Not checked — no full text of the sourcecites [12] source
• ?Not checked — no full text of the sourcecites [13] source

In the paper

“Formal search strategies, however, were used as indicated for evaluation of clinical trial information.”

In the paper

“Some of the literature review was based on the expert panel's knowledge of the field and therefore may be subject to bias.”

In the paper

“Importantly, consensus-based recommendations for standardized imaging, cognitive, and pathological protocols have been developed.”

What the sources say

• ?Not checked — no full text of the sourcecites [5] source
• ?Not checked — no full text of the sourcecites [8] source

In the paper

“the more liberal criteria for VaD proposed by Hachinski et al result in large numbers, whereas the more conservative criteria such as those of the National Institute of Neurological Disorders and Stroke–Association Internationale pour la Recherché et l'Enseignement en Neurosciences (NINDS-AIREN) yield more modest rates.”

What the sources say

• ?Not checked — no full text of the sourcecites [10] source
• ?Not checked — no full text of the sourcecites [11] source

In the paper

“Understanding of VCI has evolved substantially in recent years, based on preclinical, neuropathologic, neuroimaging, physiological, and epidemiological studies.”

In the paper

“Indeed, although Tomlinson et al described 100 mL of tissue loss as sufficient for dementia, those with lesser volumes of loss also had dementia.”

What the sources say

• ?Not checked — no full text of the sourcecites [51] source

In the paper

“these behaviors (depression or depressive symptoms) can severely influence patients’ activities of daily living and cognitive performance, although some symptoms can revert with treatment (eg, depression), and consequently cognition can improve.”

What the sources say

• ?Not checked — no full text of the sourcecites [47] source
• ?Not checked — no full text of the sourcecites [48] source

In the paper

“However, determining the volume or number necessary for VCI or dementia has proved difficult, and unlike with Alzheimer disease and other neurodegenerative diseases, there are no currently accepted neuropathological criteria to confirm a clinical diagnosis of VCI.”

In the paper

“In clinical-pathological studies, larger volumes39,51 and an increased number11,13,39,55,56 of macroscopic infarcts are as sociated with an increased likelihood of dementia.”

What the sources say

• ?Not checked — no full text of the sourcecites [39] source
• ?Not checked — no full text of the sourcecites [51] source
• ?Not checked — no full text of the sourcecites [11] source
• ?Not checked — no full text of the sourcecites [13] source
• ?Not checked — no full text of the sourcecites [55] source
• ?Not checked — no full text of the sourcecites [56] source

In the paper

“For decades it has been recognized that cerebrovascular disease is associated with dementia”

What the sources say

• ?Not checked — no full text of the sourcecites [11] source
• ?Not checked — no full text of the sourcecites [51] source

In the paper

“This research area is complicated by the difficulty of clinically differentiating Alzheimer disease or VCI from mixed (Alzheimer disease plus cerebrovascular disease) disease, which may be more common than either “pure” Alzheimer disease or “pure” VCI.”

What the sources say

• ?Not checked — no full text of the sourcecites [9] source

In the paper

“whereas primary vessel disease may be associated with focal (eg, infarct) or diffuse tissue damage (eg, white matter degeneration) or may result in nonmorphologic functional changes.”

In the paper

“One study showed that only people with Alzheimer disease pathology with subcortical infarcts had dementia, raising the possibility of an interaction (a multiplicative effect) between the 2 pathologies.”

What the sources say

• ?Not checked — no full text of the sourcecites [16] source

In the paper

“Vascular and degenerative pathologies are 2 common disorders in later life and often coexist”

In the paper

“The interplay between macroscopic and microscopic infarcts and other vascular and degenerative pathologies in the development of clinical Alzheimer disease and VCI is complex.”

In the paper

“and each separately adds to the likelihood of cognitive impairment and dementia.”

In the paper

“In addition, vascular and degenerative pathologies may result in overlapping clinical and imaging phenotypes.”

In the paper

“loss of energy-saving saltatory conduction increases metabolic demands and enhances local energy deficit and hypoxia.128”

What the sources say

• ?Not checked — no full text of the sourcecites [128] source

In the paper

“Aβ is a potent vasoconstrictor113,114 and suppresses endothelium-dependent responses, functional hyperemia, and cerebrovascular autoregulation.115–117”

What the sources say

• ?Not checked — no full text of the sourcecites [113] source
• ?Not checked — no full text of the sourcecites [114] source
• Not checked yet

  Checked before — its earlier verdict is held back until a new check runs.

  cites [115] source
• ?Not checked — no full text of the sourcecites [116] source
• ?Not checked — no full text of the sourcecites [117] source

In the paper

“Plasma Aβ, which is elevated in some patients with VCI and Alzheimer disease, induces cerebrovascular insufficiency and could play a role in the white matter alterations observed in both conditions.130,131”

What the sources say

• ?Not checked — no full text of the sourcecites [130] source
• ?Not checked — no full text of the sourcecites [131] source

In the paper

“Although free radicals can induce inflammation by activating redox-sensitive proinflammatory transcription factors, the endothelial dysfunction induced by oxidative stress can release vascular endothelial growth factor and prostanoids, which promote vascular leakage, protein extravasation, and cytokine production.125”

What the sources say

• ?Not checked — no full text of the sourcecites [125] source

In the paper

“in Alzheimer disease and CAA, accumulation of Aβ in the media of cortical arterioles weakens the vessel wall and increases the chance of lobar hemorrhages.109”

What the sources say

• ?Not checked — no full text of the sourcecites [109] source

In the paper

“Arterioles exhibit signs of “onion skin”–type changes and undergo hyaline degeneration (lipohyalinosis), a cause of microhemorrhages.105”

What the sources say

• ?Not checked — no full text of the sourcecites [105] source

In the paper

“In models of autoimmune white matter injury, extravasation of plasma protein triggers vascular inflammation and axonal demyelination,127 which in turn disrupts saltatory conduction,128 slowing the transmission of nerve impulses.”

What the sources say

• ?Not checked — no full text of the sourcecites [127] source
• ?Not checked — no full text of the sourcecites [128] source

In the paper

“CAA appears in ≈10% to 30% of unselected brain autopsies and 80% to 100% when in the presence of accompanying Alzheimer disease.136”

What the sources say

• ?Not checked — no full text of the sourcecites [136] source

In the paper

“Diagnostic approaches to CAA (and to CADASIL, the most common form of hereditary small-vessel disease) have improved, but no disease-modifying therapies have been identified.”

In the paper

“Vascular oxidative stress and inflammation underlie many of these deleterious effects and are potential therapeutic targets.”

In the paper

“Although there are relatively few animal models of cognitive impairment and white matter damage, models recapitulating features of CAA, CADASIL, cerebral hypoperfusion, and hypertensive vasculopathy have been developed, mainly in rodents.5”

What the sources say

• ?Not checked — no full text of the sourcecites [5] source

In the paper

“They include carotid wall thickening and aortic stiffening, which also likely reflect atherosclerosis and arteriosclerosis, respectively.”

In the paper

“Neurovascular dysfunction increases the brain's susceptibility to injury by (a) altering regulation of the cerebral blood supply, (b) disrupting BBB function, and (c) reducing the trophic support and repair potential of the injured brain.”

In the paper

“This disorder can present clinically as migraines with aura, mood disturbances, recurrent strokes, or cognitive impairment163 and radiographically by the appearance of extensive WMLs, lacunar infarcts, microbleeds, and brain atrophy.164”

What the sources say

• ?Not checked — no full text of the sourcecites [163] source
• ?Not checked — no full text of the sourcecites [164] source

In the paper

“CAA can also trigger vascular or perivascular inflammation,150,151 manifesting as vasogenic edema of subcortical white matter and more rapidly progressive cognitive decline.152”

What the sources say

• ?Not checked — no full text of the sourcecites [150] source
• ?Not checked — no full text of the sourcecites [151] source
• ?Not checked — no full text of the sourcecites [152] source

In the paper

“Rodent models, although well suited to genetic manipulations and large-scale studies, can be problematic because of their small amount of white matter and limited behavioral repertoire.”

In the paper

“T2*-weighted gradient-echo MRI sequences provide substantially increased sensitivity for detection of cerebral microbleeds and are key to the diagnosis of probable CAA.”

In the paper

“Other hereditary small-vessel syndromes of the brain are rare and have generally not been reported as causes of sporadic disease via de novo mutation.”

In the paper

“Central systolic blood pressure and pulse pressure can be estimated noninvasively either from the radial artery waveform, using a transfer function, or from the common carotid waveform.”

In the paper

“Furthermore, the relative contributions to VCI of microbleeds seen on MRI or microinfarcts discovered at autopsy remain uncertain, although both occur with increased frequency among people diagnosed with dementia during life.77,233”

What the sources say

• ?Not checked — no full text of the sourcecites [77] source
• ?Not checked — no full text of the sourcecites [233] source

In the paper

“Carotid IMT can reflect either a media thickening in response to the increase in blood pressure in hypertensive patients, an intima thickening in response to atherosclerotic risk factors, or most often a combination of both.”

In the paper

“In all likelihood, common cardiovascular factors influence both IMT and VCI independently, but the consequences of vascular disease may also directly affect cognitive function.”

In the paper

“Both aortic pulse wave velocity and central systolic blood pressure and pulse pressure predict cardiovascular events independent of classic cardiovascular risk factors.182”

What the sources say

• ?Not checked — no full text of the sourcecites [182] source

In the paper

“Small-vessel disease increases with age and is accelerated by vascular risk factors, most notably, hypertension and diabetes.223”

What the sources say

• ?Not checked — no full text of the sourcecites [223] source

In the paper

“As previously discussed, VCI may have a variety of clinical presentations that may depend on the setting in which patients are evaluated.”

In the paper

“The analysis of aortic pressure waveform allows the calculation of central systolic blood pressure and pulse pressure, which are influenced by aortic stiffness and the geometry and vasomotor tone of small arteries.”

In the paper

“Left hemisphere, anterior and posterior cerebral artery distribution, multiple infarcts, and strategic infarcts have been associated with PSD in at least 2 studies.40”

What the sources say

• ?Not checked — no full text of the sourcecites [40] source

In the paper

“Conversely, measures of cerebral gray matter and hippocampal volume were both associated with declines in memory performance.256”

What the sources say

• ?Not checked — no full text of the sourcecites [256] source

In the paper

“WMLs also share risk factors with stroke,239 although advancing age remains a strong effect.”

What the sources say

• ?Not checked — no full text of the sourcecites [239] source

In the paper

“Among neuroimaging findings, silent cerebral infarcts, white matter changes, and global and medial temporal lobe atrophy are associated with increased risk of PSD.252”

What the sources say

• ?Not checked — no full text of the sourcecites [252] source

In the paper

“Patients with PSD have degrees of functional impairment and high mortality rates.”

What the sources say

• ?Not checked — no full text of the sourcecites [252] source

In the paper

“In a Rochester, MN, community-based study of stroke, the prevalence of dementia was 30% immediately after stroke, and the incidence of new-onset dementia increased from 7% after 1 year to 48% after 25 years.250”

What the sources say

• ?Not checked — no full text of the sourcecites [250] source

In the paper

“WMLs are even more common and are generally present in most people >30 years of age,231 increasing steadily in extent with advancing age.”

What the sources say

• ?Not checked — no full text of the sourcecites [231] source

In the paper

“Risk of dementia is higher with increased age and fewer years of education, history of diabetes mellitus and atrial fibrillation, and recurrent stroke.251”

What the sources say

• ?Not checked — no full text of the sourcecites [251] source

In the paper

“Prevalence estimates of VaD vary widely.”

In the paper

“In general, however, after age 65 years, there is an exponential increase in prevalence and incidence of VaD as age increases,265,266 although the trends after 90 years of age have not been well established.4,267,268”

What the sources say

• ?Not checked — no full text of the sourcecites [265]
• ?Not checked — no full text of the sourcecites [266] source
• ?Not checked — no full text of the sourcecites [4] source

In the paper

“The clinical presentation and course of CVBI are highly variable, with the classic phenotype of stepwise decline in association with stroke10 being a relatively uncommon presentation for VCI.”

What the sources say

• ?Not checked — no full text of the sourcecites [10] source

In the paper

“Structural MRI provides a fairly sensitive and specific marker for CVBI, but the relationship between CVBI and cognitive impairment is confounded by the frequent presence of Alzheimer disease changes of the brain and co-occurrence of depression on a cerebrovascular basis.”

In the paper

“Antioxidants, which include vitamins E,282 C, and beta carotene,283 consumed either as a part of the diet (fruits and vegetables) or as supplements, have been reported to reduce the risk of cognitive impairment.284”

What the sources say

• ?Not checked — no full text of the sourcecites [282] source
• ?Not checked — no full text of the sourcecites [283] source
• ?Not checked — no full text of the sourcecites [284] source

In the paper

“Some studies report a higher incidence of VaD in men than in women,4,271 although a pooled analysis of incidence studies found no difference.272”

What the sources say

• ?Not checked — no full text of the sourcecites [4] source
• ?Not checked — no full text of the sourcecites [271] source
• ?Not checked — no full text of the sourcecites [272] source

In the paper

“Fish oil n-3 polyunsaturated fatty acids are of interest because of their antioxidant and antiinflammatory properties and because they are major components of membrane phospholipids in the brain and play a critical role in neuronal function.288”

What the sources say

• ?Not checked — no full text of the sourcecites [288] source

In the paper

“The apolipoprotein E ε4 allele is associated with increased levels of cardiovascular risk factors276 and is a strong indicator of genetic risk for Alzheimer disease.”

What the sources say

• ?Not checked — no full text of the sourcecites [276] source

In the paper

“MCI may not differ by sex,273 but additional studies are needed to answer this question.”

What the sources say

• ?Not checked — no full text of the sourcecites [273] source

In the paper

“The incidence of VaD appears to be higher in blacks than in whites4 or in Hispanics with a history of stroke,274 possibly reflecting group differences in cerebrovascular risk profile.”

What the sources say

• ?Not checked — no full text of the sourcecites [4] source
• ?Not checked — no full text of the sourcecites [274] source

In the paper

“Thus, there are a number of possible explanations or confounders in relation to education level and VCI.”

In the paper

“We recognize that this is a somewhat arbitrary choice, because many articles and reviews show that vascular risk factors are also importantly associated with Alzheimer disease, mixed dementia, and amnestic MCI.110,260,261”

What the sources say

• ?Not checked — no full text of the sourcecites [110] source
• ?Not checked — no full text of the sourcecites [260] source
• ?Not checked — no full text of the sourcecites [261] source

In the paper

“Findings from these prospective cohort studies for diastolic blood pressure and cognitive decline are less consistent; however, many have reported a similar inverse relation.”

In the paper

“In longitudinal cohort studies, higher systolic blood pressure has been associated with greater late-life cognitive decline, although some studies have reported a J- or U-shaped relation.342”

What the sources say

• ?Not checked — no full text of the sourcecites [342] source