scholarly journals Nutrients, Cognitive Function, and Brain Aging: What We Have Learned from Dogs

2021 ◽  
Vol 9 (4) ◽  
pp. 72
Author(s):  
Yuanlong Pan
Keyword(s):  
Cognitive Function ◽  
Brain Atrophy ◽  
Brain Aging ◽  
Morphological Changes ◽  
Nutritional Intervention ◽  
Cortical Atrophy ◽  
Amyloid Angiopathy ◽  
Ventricular Enlargement ◽  
Increased Risk ◽  
Cerebral Amyloid

Due to a difference in genetics, environmental factors, and nutrition, just like in people, dogs age at different rates. Brain aging in people and dogs share similar morphological changes including irreversible cortical atrophy, cerebral amyloid angiopathy, and ventricular enlargement. Due to severe and irreversible brain atrophy, some aging dogs develop cognitive dysfunction syndrome (CDS), which is equivalent to dementia or Alzheimer’s disease (AD) in people. The risk factors and causes of CDS in dogs have not been fully investigated, but age, gender, oxidative stress, and deficiency of sex hormones appears to be associated with increased risk of accelerated brain aging and CDS in dogs. Both AD and CDS are incurable diseases at this moment, therefore more efforts should be focused on preventing or reducing brain atrophy and minimizing the risk of AD in people and CDS in dogs. Since brain atrophy leads to irreversible cognitive decline and dementia, an optimal nutritional solution should be able to not only enhance cognitive function during aging but also reduce irreversible brain atrophy. Up to now, only one nutritional intervention has demonstrated both cognition-enhancing benefits and atrophy-reducing benefits.

scholarly journals Late-Life Vascular Risk Score in Association With Postmortem Cerebrovascular Disease Brain Pathologies

Stroke ◽  
2021 ◽  
Author(s):  
Shahram Oveisgharan ◽  
Lei Yu ◽  
Ana Capuano ◽  
Zoe Arvanitakis ◽  
Lisa L. Barnes ◽  
...  
Keyword(s):  
Cerebrovascular Disease ◽  
Cerebral Amyloid Angiopathy ◽  
Risk Score ◽  
Odds Ratio ◽  
Amyloid Angiopathy ◽  
Individual Level ◽  
Framingham Risk ◽  
Increased Risk ◽  
Cerebral Amyloid ◽  
The Individual

Background and Purpose: The general cardiovascular Framingham risk score (FRS) identifies adults at increased risk for stroke. We tested the hypothesis that baseline FRS is associated with the presence of postmortem cerebrovascular disease (CVD) pathologies. Methods: We studied the brains of 1672 older decedents with baseline FRS and measured CVD pathologies including macroinfarcts, microinfarcts, atherosclerosis, arteriolosclerosis, and cerebral amyloid angiopathy. We employed a series of logistic regressions to examine the association of baseline FRS with each of the 5 CVD pathologies. Results: Average age at baseline was 80.5±7.0 years and average age at death was 89.2±6.7 years. A higher baseline FRS was associated with higher odds of macroinfarcts (odds ratio, 1.10 [95% CI, 1.07–1.13], P <0.001), microinfarcts (odds ratio, 1.04 [95% CI, 1.01–1.07], P =0.009), atherosclerosis (odds ratio, 1.07 [95% CI, 1.04–1.11], P <0.001), and arteriolosclerosis (odds ratio, 1.04 [95% CI, 1.01–1.07], P =0.005). C statistics for these models ranged from 0.537 to 0.595 indicating low accuracy for predicting CVD pathologies. FRS was not associated with the presence of cerebral amyloid angiopathy. Conclusions: A higher FRS score in older adults is associated with higher odds of some, but not all, CVD pathologies, with low discrimination at the individual level. Further work is needed to develop a more robust risk score to identify adults at risk for accumulating CVD pathologies.

scholarly journals Amyloid Spells and High Blood Pressure: Imminent Danger

2014 ◽  
Vol 7 (1) ◽  
pp. 39-43 ◽  
Author(s):  
Andre Caetano ◽  
Miguel Pinto ◽  
Sofia Calado ◽  
Miguel Viana-Baptista
Keyword(s):  
Blood Pressure ◽  
High Blood Pressure ◽  
Cerebral Amyloid Angiopathy ◽  
Antiplatelet Agents ◽  
Pressure Profile ◽  
Clonic Seizure ◽  
Superficial Siderosis ◽  
Amyloid Angiopathy ◽  
Increased Risk ◽  
Cerebral Amyloid

We present the case of a 71-year-old male, admitted after a generalized tonic-clonic seizure, with a history of recurrent left arm and face paresthesias, associated with sulcal cortical subarachnoid hemorrhages. During the next 48 h, he remained agitated with a high blood pressure profile; he also suffered a cardiac arrest in relation to a severe left fronto-parietal and a smaller right parietal parenchymal hemorrhage that developed over the subarachnoid hemorrhage locations. There were no intracranial vascular abnormalities. Three months later, an MRI revealed disseminated superficial siderosis. He was discharged with a modified Rankin scale of 4. He died 1 month later of unknown cause. A diagnosis of probable cerebral amyloid angiopathy was assumed. Patients with pathologically proven cerebral amyloid angiopathy that present with transient focal neurological symptoms in relation to cortical bleeds, the so-called ‘myloid spells' seem to be at an increased risk of future parenchymal hemorrhages. Avoiding antiplatelet agents in these cases has been proposed. Our case suggests that these patients should be monitored closely in the hyperacute phase , and tight blood pressure control should be considered as the immediate risk of bleeding may be high, even without a definitive diagnosis of cerebral amyloid angiopathy.

Cerebral amyloid angiopathy–associated intracerebral hemorrhage: pathology and management

2012 ◽  
Vol 32 (4) ◽  
pp. E7 ◽  
Author(s):  
Prachi Mehndiratta ◽  
Sunil Manjila ◽  
Thomas Ostergard ◽  
Sylvia Eisele ◽  
Mark L. Cohen ◽  
...  
Keyword(s):  
Intracerebral Hemorrhage ◽  
Cerebral Amyloid Angiopathy ◽  
Management Strategies ◽  
Case Series ◽  
The Elderly ◽  
Postoperative Hemorrhage ◽  
Amyloid Angiopathy ◽  
Increased Risk ◽  
Cerebral Amyloid

Amyloid angiopathy–associated intracerebral hemorrhage (ICH) comprises 12%–15% of lobar ICH in the elderly. This growing population has an increasing incidence of thrombolysis-related hemorrhages, causing the management of hemorrhages associated with cerebral amyloid angiopathy (CAA) to take center stage. A concise reference assimilating the pathology and management of this clinical entity does not exist. Amyloid angiopathy–associated hemorrhages are most often solitary, but the natural history often progresses to include multifocal and recurrent hemorrhages. Compared with other causes of ICH, patients with CAA-associated hemorrhages have a lower mortality rate but an increased risk of recurrence. Unlike hypertensive arteriolar hemorrhages that occur in penetrating subcortical vessels, CAA-associated hemorrhages are superficial in location due to preferential involvement of vessels in the cerebral cortex and meninges. This feature makes CAA-associated hemorrhages easier to access surgically. In this paper, the authors discuss 3 postulates regarding the pathogenesis of amyloid hemorrhages, as well as the established clinicopathological classification of amyloid angiopathy and CAA-associated ICH. Common inheritance patterns of familial CAA with hemorrhagic strokes are discussed along with the role of genetic screening in relatives of patients with CAA. The radiological characteristics of CAA are described with specific attention to CAA-associated microhemorrhages. The detection of these microhemorrhages may have important clinical implications on the administration of anticoagulation and antiplatelet therapy in patients with probable CAA. Poor patient outcome in CAA-associated ICH is associated with dementia, increasing age, hematoma volume and location, initial Glasgow Coma Scale score, and intraventricular extension. The surgical management strategies for amyloid hemorrhages are discussed with a review of published surgical case series and their outcomes with a special attention to postoperative hemorrhage.

scholarly journals 204 Clinicoradiological Diagnosis of Cerebral Amyloid Angiopathy-Related Inflammation (CAA-ri) - a Non-Invasive Approach to Diagnosis and Management

2019 ◽  
Vol 48 (Supplement_3) ◽  
pp. iii17-iii65
Author(s):  
Deirdre McCartan ◽  
David Williams ◽  
Barry Moynihan ◽  
Karl Boyle
Keyword(s):  
Cerebral Amyloid Angiopathy ◽  
Epileptiform Activity ◽  
Brain Biopsy ◽  
Cognitive Change ◽  
Cognitive Testing ◽  
Amyloid Angiopathy ◽  
Related Disorder ◽  
Invasive Approach ◽  
Increased Risk ◽  
Cerebral Amyloid

Abstract Background Cerebral Amyloid Angiopathy (CAA) is an age-related disorder characterised by deposition of beta-amyloid protein in the walls of small and medium cortical vessels leading to increased risk of intracranial bleeding. CAA-Related Inflammation (CAA-ri) is an under recognised subtype of CAA potentially responsive to immunosuppression and traditionally diagnosed by invasive brain biopsy. CAA-ri is associated with rapid cognitive decline but shows reversibility for some when treated with immunosuppression. We present the case of an 82 year old lady who presented with first seizure, a history of notable cognitive change and neuroimaging consistent with probable CAA-ri. Methods Validated clinicoradiological diagnostic criteria for CAA-ri were applied to MRI T2 FLAIR and SWI sequences. CSF, APOE genotyping, EEG and cognitive testing were performed. Interdisciplinary perspectives were sought from Neurology, Neurosurgery and Infectious Diseases colleagues. Consensus opinion opposed brain biopsy on strength of imaging evidence and pulsed intravenous steroid treatment was initiated. BP, anti-convulsant and bone protection were optimised and anti-thrombotics avoided. Repeat imaging and cognitive testing were repeated after four months. Results MRI T2-FLAIR revealed an asymmetric multifocal distribution of cortical and subcortical white matter hyperintensities (WMH) with leptomeningeal enhancement while SWI showed extensive multifocal microhaemorrhages with confluent haemorrhage in the right frontal and temporal regions. EEG demonstrated right frontal theta slowing and absence of epileptiform activity. CSF analysis reported raised protein at 53mg/dl. Normal WCC. Formal cognitive testing with ACEIII revealed a score of 79/100. EPOA was advised. Conclusion Clinicoradiological diagnosis of CAA-ri permits early initiation of immunosuppressive therapy and avoids invasive brain biopsy. In the absence of clinical suspicion and blood sensitive imaging sequences CAA-ri may be misdiagnosed as Acute Ischaemic Stroke or TIA where the addition of anti-thrombotic therapy could cause harm while early medical management offers potential reversibility.

Cerebral amyloid angiopathy-related transient focal neurological episodes: A transient ischemic attack mimic with an increased risk of intracranial hemorrhage

2019 ◽  
Vol 406 ◽  
pp. 116452 ◽  
Author(s):  
Marta Vales-Montero ◽  
Andrés García-Pastor ◽  
Ana María Iglesias-Mohedano ◽  
Ester Esteban-de Antonio ◽  
Paula Salgado-Cámara ◽  
...  
Keyword(s):  
Cerebral Amyloid Angiopathy ◽  
Intracranial Hemorrhage ◽  
Transient Ischemic Attack ◽  
Amyloid Angiopathy ◽  
Increased Risk ◽  
Cerebral Amyloid ◽  
Ischemic Attack

Abstract W P257: Predictors of the CT Angiography Spot Sign in Deep and Lobar Intracerebral Hemorrhage

Stroke ◽  
2014 ◽  
Vol 45 (suppl_1) ◽  
Author(s):  
Farid Radmanesh ◽  
Guido J Falcone ◽  
Christopher D Anderson ◽  
Thomas W Battey ◽  
Alison M Ayres ◽  
...  
Keyword(s):  
Logistic Regression ◽  
Intracerebral Hemorrhage ◽  
Ct Angiography ◽  
Cerebral Amyloid Angiopathy ◽  
Symptom Onset ◽  
Hematoma Expansion ◽  
Amyloid Angiopathy ◽  
Spot Sign ◽  
Increased Risk ◽  
Cerebral Amyloid

Objectives: Intracerebral hemorrhage (ICH) patients with CT angiography (CTA) spot sign are at increased risk of hematoma expansion and poor outcome. Since ICH is often the acute manifestation of a chronic cerebral vasculopathy, we investigated whether different clinical or imaging characteristics predict spot sign presence in patients with different underlying vasculopathies. Using ICH location as a surrogate for hypertension-related ICH and cerebral amyloid angiopathy-related ICH, we identified risk factors associated with spot sign. METHODS: We retrospectively analyzed a prospective cohort of consecutive spontaneous ICH patients with available CTA. Spot sign presence was ascertained by two independent readers blinded to clinical data. We assessed potential predictors of spot sign be performing uni- and multivariable logistic regression, analyzing deep and lobar ICH separately. RESULTS: 649 patients were eligible, 291 (45%) deep and 358 (55%) lobar ICH. Median time from symptom onset to CTA was 4.5 (IQR 5.2) and 5.7 (IQR 7.4) hours in patients with deep and lobar ICH, respectively. At least one spot sign was present in 76 (26%) deep and 103 (29%) lobar ICH patients. In mutivariable logistic regression, independent predictors of spot sign in deep ICH were warfarin (OR 2.82 [95%CI 1.06-7.57]; p=0.03), time from symptom onset to CTA (OR 0.9 [95%CI 0.81-0.97]; p=0.02), and baseline ICH volume (OR 1.27 [95%CI 1.14-1.43]; p=2.5E-5; per 10 mL increase). Predictors of spot sign in lobar ICH were preexisting dementia (OR 2.7 [95%CI 1.15-6.43]; p=0.02), warfarin (OR 4.01 [95%CI 1.78-9.29]; p=0.009), and baseline ICH volume (OR 1.27 [95%CI 1.17-1.39]; p=5.4E-8; per 10 mL increase). As expected, spot sign presence was a strong predictor of hematoma expansion in both deep (OR 3.52 [95%CI 1.72-7.2]; p=0.0005) and lobar ICH (OR 6.53 [95%CI 3.23-13.44]; p=2.2E-7). CONCLUSIONS: The most potent associations with spot sign are shared by deep and lobar ICH, suggesting that ICH caused by different vasculopathic processes share biological features. The relationship between preexisting dementia and spot sign in lobar ICH, but not deep ICH, suggests that ICH occurring in the context of more advanced cerebral amyloid angiopathy may be more likely to have prolonged bleeding.

scholarly journals Investigation of hypertensive arteriopathy-related and cerebral amyloid angiopathy-related small vessel disease scores in patients from a memory clinic: a prospective single-centre study

BMJ Open ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. e042550
Author(s):  
Kana Matsuda ◽  
Akihiro Shindo ◽  
Yuichiro Ii ◽  
Ken-ichi Tabei ◽  
Yukito Ueda ◽  
...  
Keyword(s):  
Cognitive Function ◽  
Cerebral Amyloid Angiopathy ◽  
Small Vessel Disease ◽  
Amyloid Angiopathy ◽  
Memory Clinic ◽  
Single Centre ◽  
Vessel Disease ◽  
Single Centre Study ◽  
Cerebral Amyloid ◽  
The Relationship

ObjectiveThe severity of cerebral small vessel disease (SVD) is assessed through neuroimaging findings, including hypertensive arteriopathy (HA)-SVD and cerebral amyloid angiopathy (CAA)-SVD. HA-SVD and CAA-SVD have been collectively estimated as total scores: the HA-SVD and CAA-SVD scores, respectively. Previous reports suggest that HA-SVD scores are associated with cognitive function; however, the relationship between CAA-SVD scores and cognitive function remains unclear. Therefore, we examined the association between CAA-SVD scores and cognitive function. Furthermore, we developed a modified CAA-SVD score considering cortical microinfarcts and posterior dominant white matter hyperintensities, which are imaging findings of CAA, and examined the association between these scores and cognitive function in the same patient group.DesignProspective study.SettingSingle centre study from a memory clinic.ParticipantsSubjects were diagnosed with mild cognitive impairment (MCI) or mild dementia in our memory clinic between February 2017 and July 2019 and underwent clinical dementia rating scale and brain MRI assessment. A total of 42 patients (aged 75.3±9.12 years) were registered prospectively.Primary and secondary outcome measuresWe evaluated intellectual function, memory, frontal lobe function and constructional ability. Furthermore, the relationship between each score and cognitive function was examined.ResultsThe CAA-SVD score showed significant associations with cognitive function (R2=0.63, p=0.016), but the HA-SVD score did not (R2=0.41, p=0.35). The modified CAA-SVD score was also significantly associated with cognitive function (R2=0.65, p=0.008).ConclusionCognitive function is associated with the CAA-SVD score, and more efficiently with the modified CAA-SVD score, in memory clinic patients. Although we have not validated the weighting of the modified CAA-SVD score, these scores can be a predictor of cognitive deterioration in patients with MCI and mild dementia.

Evaluation of cognitive function in a patient with cerebral amyloid angiopathy

1995 ◽  
Vol 10 (4) ◽  
pp. 316-316
Author(s):  
P.A. Cyrus ◽  
M.H. Krengel ◽  
R. Fama ◽  
J. Knoefel ◽  
R.F. White
Keyword(s):  
Cognitive Function ◽  
Cerebral Amyloid Angiopathy ◽  
Amyloid Angiopathy ◽  
Cerebral Amyloid

scholarly journals Cortical Thickness and Its Association with Clinical Cognitive and Neuroimaging Markers in Cerebral Amyloid Angiopathy

2021 ◽  
pp. 1-9
Author(s):  
Arsenije Subotic ◽  
Cheryl R. McCreary ◽  
Feryal Saad ◽  
Amanda Nguyen ◽  
Ana Alvarez-Veronesi ◽  
...  
Keyword(s):  
Cognitive Decline ◽  
Cerebral Amyloid Angiopathy ◽  
Cortical Thickness ◽  
Vascular Reactivity ◽  
Cortical Atrophy ◽  
White Matter Hyperintensity ◽  
Amyloid Angiopathy ◽  
Healthy Controls ◽  
Normative Study ◽  
Cerebral Amyloid

Background: Cerebral amyloid angiopathy (CAA) contributes to brain neurodegeneration and cognitive decline, but the relationship between these two processes is incompletely understood. Objective: The purpose of this study is to examine cortical thickness and its association with cognition and neurodegenerative biomarkers in CAA. Methods: Data were collected from the Functional Assessment of Vascular Reactivity study and the Calgary Normative Study. In total, 48 participants with probable CAA, 72 cognitively normal healthy controls, and 24 participants with mild dementia due to AD were included. Participants underwent an MRI scan, after which global and regional cortical thickness measurements were obtained using FreeSurfer. General linear models, adjusted for age and sex, were used to compare cortical thickness globally and in an AD signature region. Results: Global cortical thickness was lower in CAA compared to healthy controls (mean difference (MD) –0.047 mm, 95% confidence interval (CI) –0.088, –0.005, p = 0.03), and lower in AD compared to CAA (MD –0.104 mm, 95% CI –0.165, –0.043, p = 0.001). In the AD signature region, cortical thickness was lower in CAA compared to healthy controls (MD –0.07 mm, 95% CI –0.13 to –0.01, p = 0.02). Within the CAA group, lower cortical thickness was associated with lower memory scores (R2 = 0.10; p = 0.05) and higher white matter hyperintensity volume (R2 = 0.09, p = 0.04). Conclusion: CAA contributes to neurodegeneration in the form of lower cortical thickness, and this could contribute to cognitive decline. Regional overlap with an AD cortical atrophy signature region suggests that co-existing AD pathology may contribute to lower cortical thickness observed in CAA.

scholarly journals Lack of association between proton pump inhibitor use and brain aging: a cross-sectional study

2021 ◽  
Author(s):  
Nayeon Ahn ◽  
Stefan Frenzel ◽  
Katharina Wittfeld ◽  
Robin Bülow ◽  
Henry Völzke ◽  
...  
Keyword(s):  
Cognitive Function ◽  
Proton Pump ◽  
Brain Aging ◽  
Verbal Learning ◽  
Brain Magnetic Resonance Imaging ◽  
Primary Analysis ◽  
Cross Sectional ◽  
Brain Volumes ◽  
Increased Risk ◽  
Brain Age

Abstract Purpose Due to conflicting scientific evidence for an increased risk of dementia by intake of proton pump inhibitors (PPIs), this study investigates associations between PPI use and brain volumes, estimated brain age, and cognitive function in the general population. Methods Two surveys of the population-based Study of Health in Pomerania (SHIP) conducted in Northeast Germany were used. In total, 2653 participants underwent brain magnetic resonance imaging (MRI) and were included in the primary analysis. They were divided into two groups according to their PPI intake and compared with regard to their brain volumes (gray matter, white matter, total brain, and hippocampus) and estimated brain age. Multiple regression was used to adjust for confounding factors. Cognitive function was evaluated by the Verbal Learning and Memory Test (VLMT) and the Nuremberg Age Inventory (NAI) and put in relation to PPI use. Results No association was found between PPI use and brain volumes or the estimated brain age. The VLMT score was 1.11 lower (95% confidence interval: − 2.06 to − 0.16) in immediate recall, and 0.72 lower (95% CI: − 1.22 to − 0.22) in delayed recall in PPI users than in non-users. PPI use was unrelated to the NAI score. Conclusions The present study does not support a relationship between PPI use and brain aging.

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