Hippocampal and amygdalar volume changes in elderly patients with Alzheimer's disease and schizophrenia

Prestia, Annapaola; Boccardi, Marina; Galluzzi, Samantha; Cavedo, Enrica; Adorni, Andrea; Soricelli, Andrea; Bonetti, Matteo; Geroldi, Cristina; Giannakopoulos, Pantéleimon; Thompson, Paul A.; Frisoni, Giovanni B.

doi:10.1016/j.pscychresns.2010.12.015

Cited by 42 publications

(32 citation statements)

References 49 publications

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“…concomitantly with hippocampal neurodegeration. Similarly, in vivo MRI studies show reduced amygdala volumes in AD patients (Barnes et al, 2006, Cavedo et al, 2011, Cavedo et al, 2011, Cuenod et al, 1993, Heun et al, 1997, Martinez-Castillo et al, 2001, Prestia et al, 2011). Moreover, studies of amygdala morphology reported a significant tissue loss in AD patients in the dorsal medial and central nuclei, and in the ventral basolateral complex (Cavedo et al, 2011, Qiu et al, 2009), in line with neuropathology.…”

Section: Introductionmentioning

confidence: 90%

Medial temporal atrophy in early and late-onset Alzheimer's disease

Cavedo

Pievani

Boccardi

et al. 2014

Neurobiology of Aging

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Late-onset and early-onset Alzhemer’s disease (LOAD, EOAD) affect different neural systems and may be separate nosographic entities. The most striking differences is in the medial temporal lobe, severely affected in LOAD and relatively spared in EOAD. We assessed amygdalar morphology and volume in 18 LOAD and 18 EOAD patients and 36 aged-matched controls, and explored their relationship with hippocampal volume. 3D amygdalar shape was reconstructed with the Radial Atrophy Mapping technique, hippocampal volume was measured using a manual method. Atrophy was greater in LOAD than EOAD: 25% versus 17% in the amygdala and 20% versus 13% in the hippocampus. In the amygdala, LOAD showed significantly greater tissue loss than EOAD in the right dorsal central, lateral, and basolateral nuclei (20-30% loss, p<0.03), all known to be connected to limbic regions. In LOAD but not EOAD, greater hippocampal atrophy was associated with amygdalar atrophy in the left dorsal central and medial nuclei (r=0.6, p<0.05), also part of the limbic system. These findings support the notion that limbic involvement is a prominent feature of LOAD but not EOAD.

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Section: Introductionmentioning

confidence: 90%

Medial temporal atrophy in early and late-onset Alzheimer's disease

Cavedo

Pievani

Boccardi

et al. 2014

Neurobiology of Aging

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“…Volume deficits in both brain regions has been documented in a variety of brain disorders, including schizophrenia (8). Progressive hippocampal and amygdalar tissue loss may occur in the course of the disease, and may reflect abnormal plasticity and neurodegeneration (9), although the contributing mechanisms are not widely agreed and the same etiology may not be found in all patients (10–11). Early case-control MRI studies of schizophrenia patients have reported structural differences including reduced volume of medial temporal lobe structures, mainly located in the hippocampus and amygdale (see (12) for a review).…”

Section: Objectivementioning

confidence: 99%

“…In addition, we previously (9) examined MRI hippocampal and amygdalar volumes as well as their asymmetries in schizophrenia patients. Moreover, medial temporal lobe alterations have been observed, to a lower extent, in the unaffected relatives of schizophrenia patients (19) representing a morphological endophenotype that could reflect a higher risk for developing schizophrenia (11), rendering the hippocampus and the amygdala two key regions for all the features of this disease.…”

Section: Objectivementioning

confidence: 99%

Hippocampal and Amygdalar Local Structural Differences in Elderly Patients with Schizophrenia

Prestia

Cavedo

Boccardi

et al. 2015

The American Journal of Geriatric Psychiatry

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Objectives Morphological abnormalities have been reported for the hippocampi and amygdalae in young schizophrenia patients, but very little is known about the pattern of abnormalities in elderly schizophrenia patients. Here we investigated local structural differences in the hippocampi and amygdalae of elderly schizophrenia patients compared to healthy elderly subjects. We also related these differences to clinical symptom severity. Design 20 schizophrenia patients (mean age: 67.4±6.2 years, MMSE 22.8±4.4) and 20 healthy elderly subjects (70.3±7.5, 29.0±1.1) underwent high resolution magnetic resonance imaging of the brain. The Radial Atrophy Mapping technique was used to reconstruct the 3D shape of the amygdala and the hippocampus. Local differences in tissue reductions were computed between groups and permutation tests were run to correct for multiple comparisons, in statistical maps thresholded at p=0.05. Results Significant tissue reduction was observed bilaterally in the amygdala and hippocampus of schizophrenia patients. The basolateral-ventral-medial amygdalar nucleus showed the greatest involvement, with over 30% local tissue reduction. The centro-medial, cortical, and lateral nuclei were also atrophic in patients. The hippocampus showed significant tissue loss in the medio-caudal and antero-lateral aspects of CA1, and in medial section of its left head (pre- and para-subiculum;). In the left amygdala and hippocampus, local tissue volumes were significantly correlated with negative symptoms. Conclusions Tissue losses and altered morphology were found in elderly schizophrenia patients. Tissue loss mapped to amygdalo-hippocampal subregions known to have bidirectional and specific connections with frontal cortical and limbic structures and was related to clinical severity.

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“…The hippocampus is especially vulnerable to brain trauma, heavy metal toxicity, inflammation and Alzheimer’s disease. Damage to the hippocampus is associated with memory loss, cognitive impairment, disorientation and mood disorders (Bekinschtein et al, 2007, Blank et al, 2002, Bolouri and Small, 2004, Dawe et al, 2011, Ekdahl et al, 2003, Femenia et al, 2012, Ishida et al, 1997, Ishikawa et al, 1997, Kesner and Williams, 1995, Kraus et al, 2010, Luft et al, 2008, Monje et al, 2003, Niedermeyer and Ghigo, 2011, Pietropaolo et al, 2007, Prestia et al, 2011, Vanderwolf, 2001). Stem cells in the hippocampus are especially vulnerable to the toxic effects of cisplatin such that treatments results in a significant depression in cell proliferation and neurogenesis (Dietrich et al, 2006, James et al, 2008, Piccolini et al, 2012, Rzeski et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

Cisplatin Inhibits Hippocampal Cell Proliferation and Alters the Expression of Apoptotic Genes

Manohar¹,

Jamesdaniel²,

Salvi³

2013

Neurotox Res

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The hippocampus, which is critical for memory and spatial navigation, contains a proliferating stem cell niche that is especially vulnerable to anti-neoplastic drugs such as cisplatin. Although the damaging effects of cisplatin have recently been recognized, the molecular mechanisms underlying its toxic effects on this vital region are largely unknown. Using a focused apoptosis gene array, we analyzed the early cisplatin-induced changes in gene expression in the hippocampus of adult Sprague-Dawley rats and compared the results to those from the inferior colliculus, a non-mitotic auditory region resistant to cisplatin-induced cell death. Two days after a 12 mg/kg dose of cisplatin, significant increases were observed in five proapoptotic genes Bik, Bid, Bok, Trp53p2 and Card6 and a significant decrease in one antiapoptotic gene Bcl2a1. In contrast, Nol3, an antiapoptotic gene showed a significant increase in expression. The cisplatin-induced increase in Bid mRNA and decrease in Bcl2a1 mRNA was accompanied by a corresponding increase and decrease of their respective proteins in the hippocampus. In contrast, the cisplatin-induced changes in Bcl2a1, Bid, Bik and Bok gene expression in the inferior colliculus were strikingly different from those in the hippocampus consistent with the greater susceptibility of the hippocampus to cisplatin toxicity. Cisplatin also significantly reduced immunolabeling of the cell proliferation marker Ki67 in the subgranular zone (SGZ) of the hippocampus two days post treatment. These results indicate that cisplatin-induced hippocampal cell death is mediated by increased expression of proapoptotic and antiapoptotic genes and proteins that likely inhibit hippocampal cell proliferation.

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Hippocampal and amygdalar volume changes in elderly patients with Alzheimer's disease and schizophrenia

Cited by 42 publications

References 49 publications

Medial temporal atrophy in early and late-onset Alzheimer's disease

Medial temporal atrophy in early and late-onset Alzheimer's disease

Hippocampal and Amygdalar Local Structural Differences in Elderly Patients with Schizophrenia

Cisplatin Inhibits Hippocampal Cell Proliferation and Alters the Expression of Apoptotic Genes

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