RETRACTED: Differential impact of diabetes and hypertension in the brain: Adverse effects in grey matter

DeVisser, Adriena; Yang, Christina; Herring, Amanda; Martinez, José A.; Rosales-Hernandez, Alma; Poliakov, Ilia; Ayer, Amit; Garven, Alexandra; Zaver, Shaila; Rincon, Natalia; Xu, Kevin; Tuor, Ursula I.; Schmidt, Ann Marie; Toth, Cory

doi:10.1016/j.nbd.2011.06.005

Cited by 35 publications

(16 citation statements)

References 45 publications

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“…In animal models of type 1 diabetes, cerebral volume loss was related to synaptic loss and loss of myelin (33). Neuronal loss was only seen in animals with both type 1 diabetes and hypertension (33). In our patient group, we previously reported axonal and myelin damage measured with diffusion tensor imaging (7), which could account for subcortical volume loss.…”

Section: Discussionmentioning

confidence: 60%

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Ventral Striatum, but Not Cortical Volume Loss, Is Related to Cognitive Dysfunction in Type 1 Diabetic Patients With and Without Microangiopathy

et al. 2014

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OBJECTIVEPatients with longstanding type 1 diabetes may develop microangiopathy due to high cumulative glucose exposure. Also, chronic hyperglycemia is related to cerebral alterations and cognitive dysfunction. Whether the presence of microangiopathy is conditional to the development of hyperglycemia-related cerebral compromise is unclear. Since subcortical, rather than cortical, volume loss was previously related to cognitive dysfunction in other populations, we measured these brain correlates and cognitive functions in patients with longstanding type 1 diabetes with and without microangiopathy. RESEARCH DESIGN AND METHODSWe evaluated differences in subcortical volume and cortical thickness and volume in type 1 diabetic patients with (n = 51) and without (n = 53) proliferative retinopathy and 49 control subjects and related volume differences to cognitive dysfunction. Analyses were corrected for age, sex, systolic blood pressure, and A1C. RESULTSPutamen and right thalamic volume loss was noted in both patients with and without proliferative retinopathy compared with control subjects (all P < 0.05). Additionally, in patients with proliferative retinopathy relative to control subjects, volume loss of the bilateral nucleus accumbens was found (all P < 0.05). No differences were observed between the two patient groups. Cortical thickness and volume were not different between groups. In pooled analyses, lower left nucleus accumbens volume was associated with cognitive dysfunction (P < 0.035). CONCLUSIONSThis study shows subcortical, but not cortical, volume loss in relation to cognitive dysfunction in patients with longstanding type 1 diabetes, irrespective of microangiopathy. The time course, pathophysiology, and clinical relevance of these findings need to be established in longitudinal and mechanistic studies.Longstanding type 1 diabetes mellitus may lead to development of microangiopathy, mediated by cumulative hyperglycemic exposure (1). Cognitive dysfunction is also related to prolonged hyperglycemia (2,3). Proliferative retinopathy, the presence of which has been found to be independently related to cognition and cerebral alterations

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Section: Discussionmentioning

confidence: 60%

“…Possible contributors include neuronal loss, axonal damage, cell death, and loss of interstitial fluids. In animal models of type 1 diabetes, cerebral volume loss was related to synaptic loss and loss of myelin (33). Neuronal loss was only seen in animals with both type 1 diabetes and hypertension (33).…”

Section: Discussionmentioning

confidence: 99%

Ventral Striatum, but Not Cortical Volume Loss, Is Related to Cognitive Dysfunction in Type 1 Diabetic Patients With and Without Microangiopathy

et al. 2014

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“…Possible subject classification confounds include the presence of diabetes in four (likely five) OSA patients, as well as the potential for undiagnosed hypertension, with both conditions associated with neural deficits [76], [77] and altered cerebral blood flow regulation in hypertension especially [78]–[80], and to some stimuli in diabetes mellitus type 2 [81]–[83]. The OSA and control groups were not matched for BMI, although the extent to which obesity influences cerebral perfusion is unclear [84].…”

Section: Discussionmentioning

confidence: 99%

Global Brain Blood-Oxygen Level Responses to Autonomic Challenges in Obstructive Sleep Apnea

et al. 2014

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Obstructive sleep apnea (OSA) is accompanied by brain injury, perhaps resulting from apnea-related hypoxia or periods of impaired cerebral perfusion. Perfusion changes can be determined indirectly by evaluation of cerebral blood volume and oxygenation alterations, which can be measured rapidly and non-invasively with the global blood oxygen level dependent (BOLD) signal, a magnetic resonance imaging procedure. We assessed acute BOLD responses in OSA subjects to pressor challenges that elicit cerebral blood flow changes, using a two-group comparative design with healthy subjects as a reference. We separately assessed female and male patterns, since OSA characteristics and brain injury differ between sexes. We studied 94 subjects, 37 with newly-diagnosed, untreated OSA (6 female (age mean ± std: 52.1±8.1 yrs; apnea/hypopnea index [AHI]: 27.7±15.6 events/hr and 31 male 54.3±8.4 yrs; AHI: 37.4±19.6 events/hr), and 20 female (age 50.5±8.1 yrs) and 37 male (age 45.6±9.2 yrs) healthy control subjects. We measured brain BOLD responses every 2 s while subjects underwent cold pressor, hand grip, and Valsalva maneuver challenges. The global BOLD signal rapidly changed after the first 2 s of each challenge, and differed in magnitude between groups to two challenges (cold pressor, hand grip), but not to the Valsalva maneuver (repeated measures ANOVA, p<0.05). OSA females showed greater differences from males in response magnitude and pattern, relative to healthy counterparts. Cold pressor BOLD signal increases (mean ± adjusted standard error) at the 8 s peak were: OSA 0.14±0.08% vs. Control 0.31±0.06%, and hand grip at 6 s were: OSA 0.08±0.03% vs. Control at 0.30±0.02%. These findings, indicative of reduced cerebral blood flow changes to autonomic challenges in OSA, complement earlier reports of altered resting blood flow and reduced cerebral artery responsiveness. Females are more affected than males, an outcome which may contribute to the sex-specific brain injury in the syndrome.

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“…Addressing these limitations will require detailed post-mortem and other in vivo (adult neurogenesis) imaging methods in order to determine those ultrastructural underpinnings. Finally, the strict exclusion criteria used in this study disallows for any judgments to be made regarding interactions between OSA and its comorbidities such as hypertension and diabetes, both strongly associated with OSA and also known to cause brain injury[2,9,71]. …”

Section: Discussionmentioning

confidence: 99%

Hippocampal Hypertrophy and Sleep Apnea: A Role for the Ischemic Preconditioning?

et al. 2013

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The full impact of multisystem disease such as obstructive sleep apnoea (OSA) on regions of the central nervous system is debated, as the subsequent neurocognitive sequelae are unclear. Several preclinical studies suggest that its purported major culprits, intermittent hypoxia and sleep fragmentation, can differentially affect adult hippocampal neurogenesis. Although the prospective biphasic nature of chronic intermittent hypoxia in animal models of OSA has been acknowledged, so far the evidence for increased ‘compensatory’ neurogenesis in humans is uncertain. In a cross-sectional study of 32 patients with mixed severity OSA and 32 non-apnoeic matched controls inferential analysis showed bilateral enlargement of hippocampi in the OSA group. Conversely, a trend for smaller thalami in the OSA group was noted. Furthermore, aberrant connectivity between the hippocampus and the cerebellum in the OSA group was also suggested by the correlation analysis. The role for the ischemia/hypoxia preconditioning in the neuropathology of OSA is herein indicated, with possible further reaching clinical implications.

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RETRACTED: Differential impact of diabetes and hypertension in the brain: Adverse effects in grey matter

Cited by 35 publications

References 45 publications

Ventral Striatum, but Not Cortical Volume Loss, Is Related to Cognitive Dysfunction in Type 1 Diabetic Patients With and Without Microangiopathy

Ventral Striatum, but Not Cortical Volume Loss, Is Related to Cognitive Dysfunction in Type 1 Diabetic Patients With and Without Microangiopathy

Global Brain Blood-Oxygen Level Responses to Autonomic Challenges in Obstructive Sleep Apnea

Hippocampal Hypertrophy and Sleep Apnea: A Role for the Ischemic Preconditioning?

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