Longitudinal changes in cognitive function and regional cerebral function in Alzheimer's disease: A SPECT blood flow study

Brown, D. B.; Hunter, Robert; Wyper, David J.; Patterson, James C.; Kelly, R.C.; Montaldi, Daniela; McCulloch, James

doi:10.1016/0022-3956(95)00032-1

Cited by 74 publications

(49 citation statements)

References 24 publications

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“…This is different from the reported findings that A␤ inhibits the ␣ 7 -nAChRs (13, 37) and ␣ 7 -nAChR-mediated cerebral vasodilation in LY pigs (40). This inhibition of ␣ 7 -nAChR-mediated vasodilation by A␤ (40) may provide a partial explanation for decreased cerebral blood flow in the early phase of AD (5,14,40), since A␤s play a key role in pathogenesis of AD. This inhibition by A␤ may also explain the upregulation of ␣ 7 -nAChR subunit protein in animal models of AD, as well as in human brain samples from AD patients (4,8,17).…”

Section: Discussioncontrasting

confidence: 83%

“…The vasodilation is blocked by ␤-amyloid peptide (A␤) via inhibition of the ␣ 7 -nAChR (40). Because A␤ is a key causative factor in pathogenesis of Alzheimer's disease (AD), A␤-inhibition of cerebral nitrergic vasodilation is consistent with the reports that AD is closely associated with reduction in regional cerebral blood flow that may accelerate the pathological progress (5,14). Accordingly, inhibition by A␤ of ␣ 7 -nAChRs on the cerebral perivascular sympathetic nerves may play a role in diminished cerebral arterial function in pathogenesis of AD (39).…”

supporting

confidence: 70%

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Sympathetic α₃β₂-nAChRs mediate cerebral neurogenic nitrergic vasodilation in the swine

Lee

Liu²,

Chen

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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Lee RH, Liu YQ, Chen PY, Liu CH, Chen MF, Lin HW, Kuo JS, Premkumar LS, Lee TJ. Sympathetic ␣3␤2-nAChRs mediate cerebral neurogenic nitrergic vasodilation in the swine. Am J Physiol Heart Circ Physiol 301: H344 -H354, 2011. First published May 2, 2011; doi:10.1152/ajpheart.00172.2011.-The ␣7-nicotinic ACh receptor (␣7-nAChR) on sympathetic neurons innervating basilar arteries of pigs crossed bred between Landrace and Yorkshire (LY) is known to mediate nicotine-induced, ␤-amyloid (A␤)-sensitive nitrergic neurogenic vasodilation. Preliminary studies, however, demonstrated that nicotine-induced cerebral vasodilation in pigs crossbred among Landrace, Yorkshire, and Duroc (LYD) was insensitive to A␤ and ␣-bungarotoxin (␣-BGTX). We investigated nAChR subtype on sympathetic neurons innervating LYD basilar arteries. Nicotine-induced relaxation of porcine isolated basilar arteries was examined by tissue bath myography, inward currents on nAChR-expressing oocytes by two-electrode voltage recording, and mRNA and protein expression in the superior cervical ganglion (SCG) and middle cervical ganglion (MCG) by reverse transcription PCR and Western blotting. Nicotine-induced basilar arterial relaxation was not affected by A␤, ␣-BGTX, and ␣-conotoxin IMI (␣7-nAChR antagonists), or ␣-conotoxin AuIB (␣3␤4-nAChR antagonist) but was inhibited by tropinone and tropane (␣3-containing nAChR antagonists) and ␣-conotoxin MII (selective ␣ 3␤2-nAChR antagonist). Nicotine-induced inward currents in ␣ 3␤2-nAChR-expressing oocytes were inhibited by ␣-conotoxin MII but not by ␣-BGTX, A␤, or ␣-conotoxin AuIB. mRNAs of ␣ 3-, ␣7-, ␤2-, and ␤4-subunits were expressed in both SCGs and MCGs with significantly higher mRNAs of ␣ 3-, ␤2-, and ␤ 4-subunits than that of ␣7-subunit. The A␤-insensitive sympathetic ␣ 3␤2-nAChR mediates nicotine-induced cerebral nitrergic neurogenic vasodilation in LYD pigs. The different finding from A␤-sensitive ␣ 7-nAChR in basilar arteries of LY pigs may offer a partial explanation for different sensitivities of individuals to A␤ in causing diminished cerebral nitrergic vasodilation in diseases involving A␤.␣ 3␤2-nicotinic ACh receptor; axo-axonal interaction; ␤-amyloid; cerebral perivascular sympathetic nerves; superior cervical ganglion IT IS WELL ESTABLISHED THAT cerebral arteries receive dense sympathetic innervation originating in the superior cervical ganglion (SCG) (24, 50) and that nicotinic ACh receptors (nAChRs) on the nerve terminals regulate norepinephrine (NE) release (50). In the pigs crossbred between Landrace and Yorkshire in the United States, activation by nicotinic agonists of the nAChRs on perivascular sympathetic nerves innervating cerebral arteries results in release of NE, which then causes release of nitric oxide (NO) from the nearby parasympathetic nitrergic nerves and dilation of the arteries (22, 39). This nicotinic agonist-induced axo-axonal interaction leading to nitrergic vasodilation is mediated by the ␣ 7 -nAChR subtype (39). The vasodilation is blocked by ␤-amyloid peptide (A␤) via inhib...

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Section: Discussioncontrasting

confidence: 83%

supporting

confidence: 70%

Sympathetic α₃β₂-nAChRs mediate cerebral neurogenic nitrergic vasodilation in the swine

Lee

Liu²,

Chen

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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“…Kurilla and Gonsalves [46] and Wolk et al [25] observed that these processes correlated with a frontal-based event-related potential (ERP) component, which is known to be associated with post-retrieval monitoring processes [47]. Importantly, pathological changes in the prefrontal cortex have been reported in Alzheimer's disease, especially in more severe patients [48,49]. Therefore, it may be that frontal lobe dysfunction in patients in a moderate stage of dementia caused impaired post-retrieval monitoring processes, leading these patients to sub-attribute fluency to prior occurrence of the item.…”

Section: Discussionmentioning

confidence: 99%

Enhancing the Salience of Fluency Improves Recognition Memory Performance in Mild Alzheimer's Disease

Bastin

Willems

Genon

et al. 2013

JAD

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Recognition memory can rely on recollection (recall of the details from the encoding episode) and familiarity (feeling that some information is old without any recollection). In Alzheimer's disease (AD), whereas there is a clear deficit of recollection, the evidence regarding familiarity is mixed, with some studies showing preserved familiarity and others reporting impairment. The current study examined whether recognition memory performance can be improved in AD when the use of familiarity is facilitated by the salience of processing fluency due to an earlier encounter with the information. Fifteen AD patients and 16 healthy controls performed a verbal recognition memory task where the salience of fluency was manipulated by means of letters overlap. Studied and unstudied words were constituted of either two separate sets of letters (no-overlap condition, high fluency salience) or the same set of letters (overlap condition, low fluency salience). The results showed that, although performance was globally poorer in AD patients than in the controls, both groups performed significantly better in the no-overlap condition than in the overlap condition. This suggests that AD patients benefited as much as the controls from the salience of fluency.

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“…Cerebral hypoperfusion predicts the development of dementia in patients with MCI and the rate of cognitive decline in patients with AD (14,16,22). The fact that the hypoperfusion actually damages the brain, even in preclinical or early disease, is well demonstrated on imaging of cerebral white matter in people with mutations that cause autosomal dominant forms of AD.…”

Section: Reduced Demand or Reduced Supply?mentioning

confidence: 91%

Cerebral Hypoperfusion and the Energy Deficit in Alzheimer's Disease

Love

Miners

2016

Brain Pathology

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Longitudinal changes in cognitive function and regional cerebral function in Alzheimer's disease: A SPECT blood flow study

Cited by 74 publications

References 24 publications

Sympathetic α₃β₂-nAChRs mediate cerebral neurogenic nitrergic vasodilation in the swine

Sympathetic α₃β₂-nAChRs mediate cerebral neurogenic nitrergic vasodilation in the swine

Enhancing the Salience of Fluency Improves Recognition Memory Performance in Mild Alzheimer's Disease

Cerebral Hypoperfusion and the Energy Deficit in Alzheimer's Disease

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Longitudinal changes in cognitive function and regional cerebral function in Alzheimer's disease: A SPECT blood flow study

Cited by 74 publications

References 24 publications

Sympathetic α3β2-nAChRs mediate cerebral neurogenic nitrergic vasodilation in the swine

Sympathetic α3β2-nAChRs mediate cerebral neurogenic nitrergic vasodilation in the swine

Enhancing the Salience of Fluency Improves Recognition Memory Performance in Mild Alzheimer's Disease

Cerebral Hypoperfusion and the Energy Deficit in Alzheimer's Disease

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Product

Resources

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Sympathetic α₃β₂-nAChRs mediate cerebral neurogenic nitrergic vasodilation in the swine

Sympathetic α₃β₂-nAChRs mediate cerebral neurogenic nitrergic vasodilation in the swine