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1.
Cortex ; 113: 15-28, 2019 04.
Article in English | MEDLINE | ID: mdl-30557760

ABSTRACT

Face-name association is a relevant ability for social interactions and involves the ventral and dorsolateral prefrontal cortices, particularly in the left hemisphere, bilateral hippocampal, fusiform gyrus and occipital regions. Previous studies demonstrated the primary role of the hippocampus for this ability in healthy subjects. However, no study has examined the participation of the left inferior frontal area, specially the left inferior frontal gyrus (LIFG) in patients with ischemic vascular lesions. In the present study we addressed this issue and investigated the neural correlates and resting state functional connectivity of face-name memory encoding in ischemic patients with LIFG or without lesions in the left IFG (nLIFG) and healthy controls (HC) using fMRI. The main results showed that the nLIFG group demonstrated efficient compensation related to encoding and performance on face-name learning and recognition memory task, in addition to similar brain areas activated during task performance compared to healthy controls. Some of these areas were more activated in nLIFG group, indicating a compensation mechanism. In contrast, the LIFG group showed worse behavior performance, and no signs of an efficient compensation mechanism. Functional connectivity analysis suggested that the left IFG region seems to be important for maintaining the connectivity of the right fusiform gyrus or, perhaps, lesion in this area is associated to maladaptive reorganization. Our findings highlight the relevant role of the left IFG in face-name learning and encoding, possibly as a primary region in addition to the bilateral hippocampal formation and fusiform gyrus.


Subject(s)
Brain Ischemia/diagnostic imaging , Facial Recognition/physiology , Names , Nerve Net/diagnostic imaging , Prefrontal Cortex/diagnostic imaging , Adult , Female , Functional Neuroimaging , Humans , Magnetic Resonance Imaging , Male , Middle Aged
2.
J Alzheimers Dis ; 55(3): 1195-1205, 2017.
Article in English | MEDLINE | ID: mdl-27792014

ABSTRACT

BACKGROUND: Recent studies report increases in neural activity in brain regions critical to episodic memory at preclinical stages of Alzheimer's disease (AD). Although electroencephalography (EEG) is widely used in AD studies, given its non-invasiveness and low cost, there is a need to translate the findings in other neuroimaging methods to EEG. OBJECTIVE: To examine how the previous findings using functional magnetic resonance imaging (fMRI) at preclinical stage in presenilin-1 E280A mutation carriers could be assessed and extended, using EEG and a connectivity approach. METHODS: EEG signals were acquired during resting and encoding in 30 normal cognitive young subjects, from an autosomal dominant early-onset AD kindred from Antioquia, Colombia. Regions of the brain previously reported as hyperactive were used for connectivity analysis. RESULTS: Mutation carriers exhibited increasing connectivity at analyzed regions. Among them, the right precuneus exhibited the highest changes in connectivity. CONCLUSION: Increased connectivity in hyperactive cerebral regions is seen in individuals, genetically-determined to develop AD, at preclinical stage. The use of a connectivity approach and a widely available neuroimaging technique opens the possibility to increase the use of EEG in early detection of preclinical AD.


Subject(s)
Alzheimer Disease/physiopathology , Alzheimer Disease/psychology , Brain Mapping , Brain/pathology , Memory, Episodic , Neural Pathways/physiology , Adult , Alzheimer Disease/epidemiology , Alzheimer Disease/genetics , Asymptomatic Diseases/epidemiology , Asymptomatic Diseases/psychology , Brain/physiopathology , Colombia/epidemiology , Diffusion Magnetic Resonance Imaging , Electroencephalography , Entropy , Female , Functional Laterality , Humans , Male , Mutation/genetics , Neuropsychological Tests , Photic Stimulation , Presenilin-1/genetics , Young Adult
3.
J Alzheimers Dis ; 47(4): 955-64, 2015.
Article in English | MEDLINE | ID: mdl-26401774

ABSTRACT

BACKGROUND: Brain regions critical to episodic memory are altered during the preclinical stages of Alzheimer's disease (AD). However, reliable means of identifying cognitively-normal individuals at higher risk to develop AD have not been established. OBJECTIVE: To examine whether functional MRI can detect early functional changes associated with scene encoding in a group of presymptomatic presenilin-1 (PSEN1) E280A mutation carriers. METHODS: Participants were 39 young, cognitively-normal individuals from an autosomal dominant early-onset AD kindred, located in Antioquia, Colombia. Participants performed a functional MRI scene encoding task and a post-scan subsequent memory test. RESULTS: PSEN1 mutation carriers exhibited hyperactivation within medial temporal lobe regions (hippocampus,parahippocampal formation) during successful scene encoding compared to age-matched non-carriers. CONCLUSION: Hyperactivation in medial temporal lobe regions during scene encoding is seen in individuals genetically-determined to develop AD years before their clinical onset. Our findings will guide future research with the ultimate goal of using functional neuroimaging in the early detection of preclinical AD.


Subject(s)
Alzheimer Disease/genetics , Alzheimer Disease/physiopathology , Brain/physiopathology , Memory/physiology , Presenilin-1/genetics , Visual Perception/physiology , Adult , Age of Onset , Alzheimer Disease/psychology , Asymptomatic Diseases , Brain Mapping , DNA Mutational Analysis , Female , Heterozygote , Humans , Magnetic Resonance Imaging , Male , Mutation , Neuropsychological Tests , Photic Stimulation
4.
Neuropharmacology ; 79: 201-11, 2014 Apr.
Article in English | MEDLINE | ID: mdl-24296155

ABSTRACT

There is general agreement that the substantial modification in memory and motivational states exerted by corticosteroids after a traumatic experience is mediated in complementary manner by the mineralocorticoid (MR) and glucocorticoid (GR) receptors. Here we tested the hypothesis that pharmacological manipulation of MR activity would affect behavioral strategy and information storage in an olfactory fear conditioning (OFC) task. Male Wistar rats were submitted to the OFC with different training intensities. We observed that following high intensity OFC acquisition, a set of defensive coping strategies, which includes avoidance and risk assessment behaviors, was elicited when subjects were exposed to the conditioned stimulus (CS) 48 h later. In addition, following either OFC acquisition or retrieval (CS-I test) a profound corticosterone secretion was also detected. Systemic administration of the MR antagonist spironolactone altered the behavioral coping style irrespective the antagonist was administered 60 min prior to the acquisition or before the retrieval session. Surprisingly, the MR agonist fludrocortisone given 60 min prior to acquisition or retrieval of OFC had similar effects as the antagonist. In addition, post-training administration of fludrocortisone, following a weak training procedure, facilitated the consolidation of OFC. Fludrocortisone rather than spironolactone reduced serum corticosterone levels, suggesting that, at least in part, the effects of the MR agonist may derive from additional GR-mediated HPA-axis suppression. In conclusion, the present study suggests the involvement of the MR in the fine-tuning of behavioral adaptation necessary for optimal information storage and expression, as revealed by the marked alterations in the risk assessment behavior.


Subject(s)
Conditioning, Psychological/drug effects , Fear/drug effects , Memory/drug effects , Mineralocorticoid Receptor Antagonists/pharmacology , Olfactory Perception/drug effects , Receptors, Mineralocorticoid/agonists , Animals , Conditioning, Psychological/physiology , Corticosterone/blood , Fear/physiology , Fludrocortisone/pharmacology , Male , Memory/physiology , Motor Activity/drug effects , Olfactory Perception/physiology , Rats , Rats, Wistar , Receptors, Mineralocorticoid/metabolism , Spironolactone/pharmacology
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