Critically attained threshold of cerebral hypoperfusion: the CATCH hypothesis of Alzheimer’s pathogenesis

Torre, Jack C. de la

doi:10.1016/s0197-4580(00)00111-1

Cited by 257 publications

(173 citation statements)

References 98 publications

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“…14 As a result of cerebral hypoperfusion, brain atrophy may occur. 15,16 Experimental evidence from animal models indeed suggests that cerebral hypoperfusion leads to cerebral microvascular damage, neuropathologic processes, and cognitive dysfunction, supporting the concept that cerebral hypoperfusion causes neurodegeneration. 17,18 Yet, the majority of studies in human subjects linking CBF to brain atrophy had a cross-sectional design, precluding unraveling cause and effect in the association.…”

Section: Introductionmentioning

confidence: 93%

The Bidirectional Association between Reduced Cerebral Blood Flow and Brain Atrophy in the General Population

Zonneveld

Loehrer

Hofman

et al. 2015

J Cereb Blood Flow Metab

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The question remains whether reduced cerebral blood flow (CBF) leads to brain atrophy or vice versa. We studied the longitudinal relation between CBF and brain volume in a community-dwelling population. In the Rotterdam Study, 3011 participants (mean age 59.6 years (s.d. 8.0)) underwent repeat brain magnetic resonance imaging to quantify brain volume and CBF at two time points. Adjusted linear regression models were used to investigate the bidirectional relation between CBF and brain volume. We found that smaller brain volume at baseline was associated with a steeper decrease in CBF in the whole population (standardized change per s.d. increase of total brain volume (TBV) = 0.296 (95% confidence interval (CI) 0.200; 0.393)). Only in persons aged ⩾ 65 years, a lower CBF at baseline was associated with steeper decline of TBV (standardized change per s.d. increase of CBF = 0.003 (95% CI − 0.004; 0.010) in the whole population and 0.020 (95% CI 0.004; 0.036) in those aged ⩾ 65 years of age). Our results indicate that brain atrophy causes CBF to decrease over time, rather than vice versa. Only in persons aged 465 years of age did we find lower CBF to also relate to brain atrophy.

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Section: Introductionmentioning

confidence: 93%

The Bidirectional Association between Reduced Cerebral Blood Flow and Brain Atrophy in the General Population

Zonneveld

Loehrer

Hofman

et al. 2015

J Cereb Blood Flow Metab

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“…4) Memory impairment emerges when the cholinergic neurons are damaged. The brain is unable to maintain its normal cell function, and cascade reaction would occur if perfusion pressure drops to a certain extent.…”

Section: Discussionmentioning

confidence: 99%

Executive Dysfunction in Patients With Cerebral Hypoperfusion After Cerebral Angiostenosis/Occlusion

Zhao

Tian

Liu

et al. 2013

Neurol. Med. Chir.(Tokyo)

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Impairment of executive functions (EFs) was investigated in patients with cerebral hypoperfusion after cerebral angiostenosis/occlusion. Several EFs were measured in patients with cerebral angiostenosis/occlusion and healthy subjects. The vascular conditions, regional cerebral blood flow (rCBF), regional cerebral blood volume (rCBV), mean transit time (MTT), time to peak (TTP), and delay time were assessed. The scores of the vascular stenosis/occlusion group were significantly lower than those of the control group. rCBV and rCBF were negatively correlated with the error response times in the Stroop test, and the persistent error responses in the Wisconsin Card Sorting Test (WCST) were positively correlated with the Montreal Cognitive Assessment (MoCA) scores. TTP was positively correlated with the reaction and error reaction times, and the persistent error response in WCST was negatively correlated with the times of sorting in WCST and MoCA scores. MTT was positively correlated with the persistent error response in WCST. In the Stroop test, delay time was positively correlated with response time, and negatively correlated with error response times, and the persistent error response in WCST and MoCA scores. Patients with cerebral hypoperfusion after cerebral angiostenosis/occlusion had executive dysfunctions in working memory, sustained attention, response inhibition, cognitive flexibility, thought organization, planning, and implementation. Moreover, their executive dysfunctions were related with the decline in rCBF and rCBV. The prolonged TTP, MTT, and delay time suggested a slow blood flow and the poor compensation of collateral circulation, resulting in impairment of the EFs.

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“…A permanent accumulation of oxidative stress products may sustain a vicious circle in which brain damage is accelerated and the blood brain barrier is compromised. Altered cellular metabolism and oxidative stress within AD-related cerebral hypoperfusion, in the presence of vascular risk factors, might favor the reach of a critical threshold for cerebral hypoperfusion (de la Torre 2000(de la Torre , 2013. The resulting increase in oxidative stress might damage the neurovascular unit and the endothelium of brain vessels thereby favoring Ab formation and nourishing a vicious circle in which plaque-induced ROS formation also damages the neurovascular unit through the endothelium (Vagnucci and Li 2003).…”

Section: Why Do We Need To Care About Dementiamentioning

confidence: 99%

“…These hypotheses share in common both coexistence of multiple-usually two-pathophysiological factors and rationale and scientific success. At the end of the 1990s, de La Torre (2000) proposed that advanced aging in the presence of a vascular risk factor may accelerate the achievement of a critical threshold of cerebral hypoperfusion (critically attained threshold of cerebral hypoperfusion, CATCH). The CATCH may trigger regional brain microcirculatory disturbance thereby impairing the adequate delivery energy substrates for normal cerebral function.…”

Section: Reflection Points For Future Researchmentioning

confidence: 99%

Nutritional contributions to dementia prevention: main issues on antioxidant micronutrients

Polidori

Schulz

2014

Genes Nutr

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There is an impressing body of evidence supporting the beneficial role of balanced nutrition in lowering the risk of dementia and its commonest form, Alzheimer's disease. Nevertheless, and despite worldwide dementia epidemic, there is much unfounded skepticism and lack of information among physicians. As a result, the diagnosis of cognitive impairment occurs still far too late, at best symptomatic drugs keep being prescribed and patients and caregivers are left with little concrete support in the hands of the natural history of the disease. This review summarizes knowledge about the impact of nutrition as part of a healthy lifestyle and of micronutrients in particular on delaying and avoiding dementia onset.Why do we need to care about dementia Dementia is the most prevalent neurodegenerative disorder, and it is characterized by progression, multiple etiology, complex symptomatology including that related to a disturbance of cognitive performance and absence of a cure. During the course of the disease, the cognitive symptoms of dementia persist and steadily worsen and behavioral disturbances appear and progress and as a result intellectual and social abilities are affected enough to obstacle the performance of activities of daily living. According to dementia definition, a diagnosis of dementia can be done when the impairment of more cognitive domains lasts long enough and is associated with behavioral disturbances both affecting activities of daily living. Dementia is indeed associated with disability and a high grade of dependence on caregivers-usually family members. This condition of disability and dependence brings along an enormous social and economic burden which is linked to the epidemics of dementia and its commonest, untreatable form, Alzheimer's disease (AD). The major risk factor for dementia and AD is advanced age, and therefore, the societal impact of AD is increasing according to aging demographics (http:// ec.europa.eu/health/reports/european). Life expectancy at birth in the EU increased from 72 years in 1980 to 78 years in 2007. The population of industrialized countries progressed from a mean life expectancy of 35 years at the beginning of the last century, to currently over 80 years of age. People aged 65 years or older are expected to double between 1995 and 2050 to reach 135 million in the EU, with very old people, aged 80 years and older, being projected to grow as much as eight to ten times on the global scale by 2050. This will strongly impact the already challenging number of ten million AD cases in the EU. As a cure against dementia has not been found yet, health care professionals all over the world are predicted to face the diagnostic, therapeutic and socioeconomical challenges of over 115 million people with dementia by 2050 (Prince et al. 2013). This perspective might be even underestimated, particularly due to inadequate diagnosis, lack of awareness and low education. The dramatic loss of synapses and cholinergic neurons, accumulation of extracellular b amyloid (Ab) plaqu...

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Critically attained threshold of cerebral hypoperfusion: the CATCH hypothesis of Alzheimer’s pathogenesis

Cited by 257 publications

References 98 publications

The Bidirectional Association between Reduced Cerebral Blood Flow and Brain Atrophy in the General Population

The Bidirectional Association between Reduced Cerebral Blood Flow and Brain Atrophy in the General Population

Executive Dysfunction in Patients With Cerebral Hypoperfusion After Cerebral Angiostenosis/Occlusion

Nutritional contributions to dementia prevention: main issues on antioxidant micronutrients

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