Abstract:Cholecystokinin (CCK) is a peptide that can be found in the cerebral cortex in high concentrations and is involved in learning and memory as well as neurodegenerative processes. Cortical brain samples from 9 patients with Alzheimer's disease and 9 matched control cases were studied with respect to the concentrations of various molecular forms of CCK and the CCK receptor binding characteristics. No differences were found between patients and controls in any of these measures. Significant correlations were found… Show more
“… 38 , 39 , 40 Low levels of CCK are found in AD patient brains and in aged and AD model mice with impaired memory. 22 , 41 , 42 , 43 Here, we found that surgery/anesthesia‐induced cognitive impairment in aged mice, and significantly decreased the levels of CCK‐8 in the hippocampus, especially in CA1 and DG regions. These results indicated that postoperative cognitive impairment was accompanied by a decrease in CCK‐8 levels in the hippocampus, which is consistent with the above‐mentioned reports on cognitive decline.…”
Section: Discussionmentioning
confidence: 59%
“…[38][39][40] Low levels of CCK are found in AD patient brains and in aged and AD model mice with impaired memory. 22,[41][42][43] Here, Synapses are basic information processing units in the brain. 44,45 The correct number and type of synaptic connections are essential for normal CNS functions.…”
This is an open access article under the terms of the Creat ive Commo ns Attri bution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
“… 38 , 39 , 40 Low levels of CCK are found in AD patient brains and in aged and AD model mice with impaired memory. 22 , 41 , 42 , 43 Here, we found that surgery/anesthesia‐induced cognitive impairment in aged mice, and significantly decreased the levels of CCK‐8 in the hippocampus, especially in CA1 and DG regions. These results indicated that postoperative cognitive impairment was accompanied by a decrease in CCK‐8 levels in the hippocampus, which is consistent with the above‐mentioned reports on cognitive decline.…”
Section: Discussionmentioning
confidence: 59%
“…[38][39][40] Low levels of CCK are found in AD patient brains and in aged and AD model mice with impaired memory. 22,[41][42][43] Here, Synapses are basic information processing units in the brain. 44,45 The correct number and type of synaptic connections are essential for normal CNS functions.…”
This is an open access article under the terms of the Creat ive Commo ns Attri bution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
“…Decreased cholecystokinin within areas such as the prefrontal cortex, amygdala and hippocampus are associated with learning and memory deficits [212]. Cholecystokinin immunoreactivity is decreased in human Alzheimer's disease brain [213] and cholecystokinin analogues prevent cholinergic degeneration in the rat cerebral cortex in an animal model of Alzheimer's disease [214]. Moreover, an age-associated decrease in cortical cholecystokinin concentration may underlie the learning and memory deficits attributable to normal aging in rodents and humans [215,216].…”
Section: Mechanism(s) Of Action Of Angiotensin IV Through Interactionmentioning
For decades, angiotensin (Ang) II was considered as the end product and the only bioactive peptide of the renin-angiotensin system (RAS). However, later studies revealed biological activity for other Ang fragments. Amongst those, Ang IV has drawn a lot of attention since it exerts a wide range of central and peripheral effects including the ability to enhance learning and memory recall, anticonvulsant and anti-epileptogenic properties, protection against cerebral ischemia, activity at the vascular level and an involvement in atherogenesis. Some of these effects are AT(1) receptor dependent but others most likely result from the binding of Ang IV to insulin-regulated aminopeptidase (IRAP) although the exact mechanism(s) of action that mediate the Ang IV-induced effects following this binding are until now not fully known. Nevertheless, three hypotheses have been put forward: since Ang IV is an inhibitor of the catalytic activity of IRAP, its in vivo effects might result from a build-up of IRAP's neuropeptide substrates. Second, IRAP is co-localized with the glucose transporter GLUT4 in several tissue types and therefore, Ang IV might interact with the uptake of glucose. A final and more intriguing hypothesis ascribes a receptor function to IRAP and hence an agonist role to Ang IV. Taken together, it is clear that further work is required to clarify the mechanism of action of Ang IV. On the other hand, a wide range of studies have made it clear that IRAP might become an important target for drug development against different pathologies such as Alzheimer's disease, epilepsy and ischemia.
“…While CCK-B receptor binding does not differ in cognitively normal vs. AD patients (Löfberg, et al, 1996), regional differences in post-mortem CCK concentration suggest an AD-like pattern of decreased expression (Mazurek and Beal, 1991). Thus, we examined if levels of CSF CCK were associated with onset and severity across the AD spectrum, and determined if CCK was related to AD-like changes in cognition, neuroimaging, and classic AD biomarkers like Aβ and tau.…”
Cholecystokinin (CCK) is a satiety hormone that is highly expressed in brain regions like the hippocampus. CCK is integral for maintaining or enhancing memory, and thus may be a useful marker of cognitive and neural integrity in participants with normal cognition, mild cognitive mpairment (MCI), and Alzheimer's disease (AD). CSF CCK levels were examined in 287 subjects from the Alzheimer's Disease Neuroimaging Initiative (ADNI). Linear or voxel-wise regression was used to examine associations between CCK, regional gray matter (GM), CSF AD biomarkers, and cognitive outcomes. Briefly, higher CCK was related to a decreased likelihood of having MCI or AD, better global and memory scores, and more GM volume primarily spanning posterior cingulate cortex, parahippocampal gyrus, and medial prefrontal cortex. CSF CCK was also strongly related to higher CSF total tau (R2=0.339) and p-tau181 (R2=0.240), but not Aβ1-42. Tau levels partially mediated CCK and cognition associations. In conclusion, CCK levels may reflect compensatory protection as AD pathology progresses.
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