Small Vessel Disease and Memory Loss: What the Clinician Needs to Know to Preserve Patients’ Brain Health

Schenk, Christian; Wuerz, Timothy; Lerner, Alan J.

doi:10.1007/s11886-013-0427-6

Cited by 6 publications

(16 citation statements)

References 180 publications

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“…Small vessel disease is best defined pathologically, although this includes a variety of microscopic findings including reduced vessel caliber, reduced vessel number, lipohyalinosis, and small cerebral infarcts. Vessel caliber is itself non-specific and may be related to lipohyalinosis, amyloid angiopathy, thrombosis leading to ischemia and infarction, and other causes [34][35][36].…”

Section: Small Vessel Disease and The Aging Brainmentioning

confidence: 99%

“…Evidence of small vessel disease found on MRI may relate to various findings: small lacunar infarcts, primary demyelinating lesions caused by many inflammatory diseases of the CNS, and periventricular or deep white matter lesions, with or without brainstem lesions. The most common locations for small vessel disease lesions include the frontal lobe, basal ganglia, and thalamo-cortical areas of the brain [34]. SVD may also be related to changes in specific white matter tracts such as are commonly seen early in degenerative disorders, affecting the inferior fronto-occipital fasciculus and causing white matter changes adjacent to the cerebral ventricles [37].…”

Section: Small Vessel Disease and The Aging Brainmentioning

confidence: 99%

“…Thus, they range from a single asymptomatic lesion to dozens or even hundreds of lesions, especially in persons with advanced cerebral amyloid angiopathy (CAA). CAA is often considered as a pathological form of small vessel disease, but is beyond the resolution of MRI, and often diagnosed indirectly based on microbleeds or symptomatic cerebral hemorrhage in older individuals occurring in locations not considered typical for hypertension-related cerebral hemorrhage [34,46]. The presence of > 4 microbleeds has been associated with amyloid-related imaging abnormalities (edema or hemorrhage), and may be symptomatic in the setting of amyloid-lowering drugs, and occurs especially in those with an APO E e4 allele [47].…”

Section: Small Vessel Disease and The Aging Brainmentioning

confidence: 99%

“…As the SVD burden increases over long periods of time, there is a correlation with increased cortical and hippocampal neuronal loss leading to global atrophy. MRI cannot detect neuronal loss which is the hallmark of atrophy, but is very sensitive to reductions in parenchymal volume, and FLAIR sequences are very sensitive to changes in white matter, albeit nonspecific as to etiology [34,43,44,48,49].…”

Section: Small Vessel Disease and The Aging Brainmentioning

confidence: 99%

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Blood Pressure Control and Protection of the Aging Brain

Wahidi

Lerner

2019

Neurotherapeutics

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Hypertension and dementia are both common disorders whose prevalence increases with age. There are multiple mechanisms by which hypertension affects the brain and alters cognition. These include blood flow dynamics, development of large and small vessel pathology and diverse molecular mechanisms including formation of reactive oxygen species and transcriptional cascades. Blood pressure interacts with Alzheimer disease pathology in numerous and unpredictable ways, affecting both β-amyloid and tau deposition, while also interacting with AD genetic risk factors and other metabolic processes. Treatment of hypertension may prevent cognitive decline and dementia, but methodological issues have limited the ability of randomized clinical trials to show this conclusively. Recent studies have raised hope that hypertension treatment may protect the function and structure of the aging brain from advancing to mild cognitive impairment and dementia.

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Section: Small Vessel Disease and The Aging Brainmentioning

confidence: 99%

Section: Small Vessel Disease and The Aging Brainmentioning

confidence: 99%

Section: Small Vessel Disease and The Aging Brainmentioning

confidence: 99%

Section: Small Vessel Disease and The Aging Brainmentioning

confidence: 99%

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Blood Pressure Control and Protection of the Aging Brain

Wahidi

Lerner

2019

Neurotherapeutics

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“…LA has become a conventional prognosis in describing cognitive dysfunction, stroke injury, cerebral small vessel disease, and neurodegenerative disorders (1,2). Increasing evidences show that more than 40% of apparently healthy adults over 50 years old present with the characteristics of high-intensity LA (3). LA has gradually become an important global health problem.…”

Section: ' Introductionmentioning

confidence: 99%

Claudin-1 and Claudin-3 as Molecular Regulators of Myelination in Leukoaraiosis Patients

Chen

Zhang

Mei

et al. 2021

Clinics

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Leukoaraiosis is described as white matter lesions that are associated with cognitive dysfunction, neurodegenerative disorders, etc. Myelin depletion is a salient pathological feature of, and the loss of oligodendrocytes is one of the most robust alterations evident in, white matter degeneration. Recent studies have revealed that claudin proteins are aberrantly expressed in leukoaraiosis and regulate oligodendrocyte activity. However, the roles of claudin-1 and claudin-3 in oligodendrocytes and leukoaraiosis are still not well-defined. METHODS: Quantitative polymerase chain reaction was used to measure the expression of claudin-1 (CLDN1), claudin-3 (CLDN3), and myelinogenesis-related genes such as myelin basic protein (MBP), proteolipid protein (PLP), oligodendrocyte transcription factor 2 (OLIG2), and SRY-box transcription factor 10 (SOX10) in leukoaraiosis patients (n=122) and healthy controls (n=122). The expression of claudin-1 and claudin-3 was either ectopically silenced or augmented in Oli-neu oligodendrocytes, and colony formation, apoptosis, and migration assays were performed. Finally, the expression of myelin proteins was evaluated by western blotting. RESULTS: Our results revealed that in addition to SOX10, the expression levels of claudin-1, claudin-3, and myelinogenesis-related proteins were prominently downregulated in leukoaraiosis patients, compared to those in healthy controls. Furthermore, the growth and migration of Oli-neu cells were downregulated upon silencing claudin-1 or claudin-3. However, the overexpression of claudin-1 or claudin-3 resulted in the reduction of the degree of apoptosis in Oli-neu cells. In addition, claudin-1 and claudin-3 promoted the expression of MBP, OLIG2, PLP, and SOX10 at the translational level. CONCLUSION: Our data has demonstrated that the abnormal expression of claudin-1 and claudin-3 regulates the pathological progression of leukoaraiosis by governing the viability and myelination of oligodendrocytes. These findings provide novel insights into the regulatory mechanisms underlying the roles of claudin-1 and claudin-3 in leukoaraiosis.

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Parietal and occipital leukoaraiosis due to cerebral ischaemic lesions decrease the driving safety performance of healthy older adults

Oba

Park

Yamashita

et al. 2022

Sci Rep

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Leukoaraiosis, a common ischaemic lesion diagnosed using magnetic resonance imaging (MRI), can influence driving safety performance (DSP). Most older drivers with leukoaraiosis are unaware of their affliction. Japan is a super-aged country, where preventing accidents caused by older drivers is an urgent national issue. We investigated the subcortical and periventricular leukoaraiosis regions that were most involved in DSP decline. The driving skills of 101 drivers (49 men, 52 women; mean age, 77.88 ± 3.77 years) without dementia were assessed by official driving instructors, using actual vehicles on a closed-circuit course. Parietal and occipital (but not frontal or temporal) leukoaraiosis volumes were significantly correlated with decreased DSP scores regardless of age, especially when turning right at intersections, which needs more attention than turning left because left-side driving is legally enforced in Japan. Occipital leukoaraiosis was also involved via a decline in dynamic visual cognitive function. MRI-based assessment of leukoaraiosis volume and localisation may enable the identification of older drivers prone to DSP deterioration. Risk factors for leukoaraiosis include smoking and lifestyle-related diseases such as hypertension. Thus, brain healthcare in patients with MRI-diagnosed leukoaraiosis may be particularly useful for the risk management of traffic accidents caused by the elderly in Japan.

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Small Vessel Disease and Memory Loss: What the Clinician Needs to Know to Preserve Patients’ Brain Health

Cited by 6 publications

References 180 publications

Blood Pressure Control and Protection of the Aging Brain

Blood Pressure Control and Protection of the Aging Brain

Claudin-1 and Claudin-3 as Molecular Regulators of Myelination in Leukoaraiosis Patients

Parietal and occipital leukoaraiosis due to cerebral ischaemic lesions decrease the driving safety performance of healthy older adults

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