Increased Neurofibrillary Tangles in Patients With Alzheimer Disease With Comorbid Depression

Rapp, Michael A.; Schnaider‐Beeri, Michal; Purohit, Dushyant P.; Perl, Daniel P.; Haroutunian, Vahram; Sano, Mary

doi:10.1097/jgp.0b013e31816029ec

Cited by 157 publications

(128 citation statements)

References 34 publications

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“…The structural integrity of microtubules is the basis of nutrient transport between the nerve cell body and axons in nerve cells. A large number of clinical-pathological studies have shown that there is a parallel relationship between neuronal density containing neurofibrillary tangles in the joint cortex and the degree of dementia (Rapp et al, 2008(Rapp et al, , 2010. In this study, we did not find typical apoptotic bodies by TEM, suggesting that apoptosis may occur at an earlier stage.…”

contrasting

confidence: 37%

Mechanisms of cytotoxicity induced by the anesthetic isoflurane: the role of inositol 1,4,5-trisphosphate receptors

Wh¹,

Zhao²,

S-P³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. Isoflurane can induce widespread cytotoxicity. We hypothesized that isoflurane induces apoptosis partly by causing excessive calcium release from the endoplasmic reticulum (ER) via direct activation of inositol 1,4,5-trisphosphate receptors (IP 3 R). Rat pheochromocytoma cells cultured for seven days with nerve growth factor were divided into four groups: control group (C), IP 3 R antagonist group (X), isoflurane group (I) and isoflurane + IP 3 R antagonist group (I+X). Groups I and I+X were treated with 1 MAC isoflurane for 12 h. Groups X and I+X were pretreated with IP 3 R antagonist. Annexin V/PI apoptosis and TUNEL assays were performed to evaluate cell apoptosis. TEM was used to observe changes in cell ultrastructure. Changes in ] i increased in groups I and I+X (P < 0.05). Compared to group C, IP 3 R mRNA expression was lower in group X and higher in group I (P < 0.05). Compared to group X, cell apoptosis rate, [Ca 2+ ] i and IP 3 R mRNA expression increased in groups I and I+X (P < 0.05). Compared to group I, cell apoptosis rate, [Ca 2+ ] i and IP 3 R mRNA expression decreased in group I+X (P < 0.05). These results suggest that exposure to 1 MAC isoflurane for 12 h causes excessive calcium release partly by direct activation of IP 3 R on the ER membrane and triggers cell apoptosis.

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contrasting

confidence: 37%

Mechanisms of cytotoxicity induced by the anesthetic isoflurane: the role of inositol 1,4,5-trisphosphate receptors

Wh¹,

Zhao²,

S-P³

et al. 2015

Genet. Mol. Res.

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“…For instance, it has been observed that late-onset depression is associated with Alzheimer's disease (AD) pathology [32] and cerebrovascular disease [33]. Therefore, we analyzed all brain specimens for the classic neuropathological lesions that are associated with AD and vascular disease pathology (e.g., plagues, tangles, and multiinfarcts), and the results from our chi-squared analyses did not produce significant differences between the depressed and non-depressed PD subjects.…”

Section: Discussionmentioning

confidence: 99%

The neuropathological basis for depression in Parkinson's disease

Frisina

Haroutunian

Libow

2009

Parkinsonism & Related Disorders

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128

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Depression is found in 30-40% of all patients with Parkinson's disease (PD), but its etiology is unclear. Using neuropathology as a signpost for neurotransmitter function, we investigated the prevalence of pathological features found at postmortem and sought to uncover differences between depressed (n = 11) and non-depressed (n = 9) elderly PD patients. The results indicate a higher prevalence of pathological features in depressed compared to non-depressed PD patients, particularly in catecholamine areas of the brain; the locus coeruleus (neuronal loss: odds ratio = 7.2, p = 08; gliosis: odds ratio = 18.0, p = 008); dorsal vagus nerve (gliosis: odds ratio = 7.63, p < 0.05), and substantia nigra pars compacta (gliosis: odds ratio 2.85, ns). However, neuropathological differences were absent in the dorsal raphe nuclei, amygdala, and cortical regions. Our evidence suggests that depression in PD is related more to catecholaminergic than serotonergic system dysfunction.

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“…We think it is less likely that the more severe depressive symptoms simply reflect a more advanced disease stage, as one would expect depressive feelings more prominently early on in the disease. Furthermore, pathologically, depression is thought to be multifactorial and heterogeneous and has also been linked to more severe AD pathology [25,26] and cerebrovascular disease [27].…”

Section: Discussionmentioning

confidence: 99%

Dementia and Rapid Mortality: Who is at Risk?

Staekenborg

Pijnenburg

Lemstra

et al. 2016

JAD

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Abstract.Background: Dementia is typically known for its insidious onset and slowly progressive course, but a subgroup deteriorates fast and dies within years or even months. Objective: The purpose of this study was to characterize dementia patients with a rapidly progressive course to death and evaluate their cause of death. Methods: We retrospectively included all patients from the Amsterdam Dementia Cohort who died within two years after diagnosis. We evaluated the characteristics of these rapid progressors and compared them to patients known to be alive two years after diagnosis ('non-rapid mortality'). Results: We included 129 dementia patients (13% of our total cohort with known follow-up) with rapid mortality (age 72 ± 10 y [29% <65 y], 70[55%]M, MMSE 20 ± 5). Mean(SD) survival was 12 ± 7 months. Compared to non-rapid mortality patients (n = 892; age 68 ± 9, 503(56%)M, MMSE 22 ± 5), patients with rapid mortality were slightly older at time of diagnosis, had lower MMSE scores, more depressive symptoms and higher prevalence of a cardiovascular history (all p < 0.05). Alzheimer's disease (AD, 43%) was most frequent in patients with rapid mortality, but the occurrence was much lower compared to non-rapid mortality patients (71%), while all other dementia diagnoses, especially Creutzfeldt-Jakob disease (CJD), vascular dementia (VaD), and frontotemporal dementia (FTD), were more frequent (p < 0.001). There were no specific characteristics for AD patients with rapid versus non-rapid mortality, especially APOE genotypes and CSF-profiles were comparable (p > 0.70). Cause of death was highly variable without a clear relation to dementia diagnosis, with exception of dementia itself in CJD, intracerebral hematoma in VaD, and motor neuron disease in FTD. Conclusions: Short survival is relatively common (∼13% in our cohort) and occurs in all different types of dementia, with overrepresentation of non-AD dementias like CJD, VaD, and FTD.

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Increased Neurofibrillary Tangles in Patients With Alzheimer Disease With Comorbid Depression

Cited by 157 publications

References 34 publications

Mechanisms of cytotoxicity induced by the anesthetic isoflurane: the role of inositol 1,4,5-trisphosphate receptors

Mechanisms of cytotoxicity induced by the anesthetic isoflurane: the role of inositol 1,4,5-trisphosphate receptors

The neuropathological basis for depression in Parkinson's disease

Dementia and Rapid Mortality: Who is at Risk?

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