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Clinical Rehabilitation Jul 2016To establish what aspects of group-based cognitive rehabilitation for memory problems are reported, and to develop a checklist for authors, which may to improve... (Review)
Review
OBJECTIVE
To establish what aspects of group-based cognitive rehabilitation for memory problems are reported, and to develop a checklist for authors, which may to improve reporting of these interventions in future studies.
DATA SOURCES
A systematic search was conducted on Web of Knowledge, CINAHL, MEDLINE, AMED, EMBASE and PsycINFO electronic databases (last search: 01/05/2015).
REVIEW METHODS
Articles were included if the sample were adults with a neurological disorder, the intervention was group-based cognitive rehabilitation for memory problems, and if the study was a randomised controlled trial. Articles were independently screened for inclusion and data extracted by two researchers, with the third researcher arbitrating any disputes.
RESULTS
Fourteen studies were included in this review. The reporting of certain aspects of an intervention was found to be poor, particularly in relation to: duration of the programme (6 of 14 studies did not report), the development of the intervention (7 of 14 studies did not discuss), and the content and structure of intervention (7 of the 14 studies did not provide details).
CONCLUSION
This review found that the overall reporting of memory rehabilitation content and format is poor. Refinement and adaption of pre-existing checklists to capture aspects of cognitive rehabilitation programmes may help authors when reporting complex interventions. A draft checklist is provided that could be refined and validated in further research.
Topics: Humans; Memory Disorders; Psychotherapy, Group
PubMed: 26229110
DOI: 10.1177/0269215515595273 -
Journal of Affective Disorders Apr 2024Schizophrenia and bipolar disorder are associated with neurocognitive and social-cognitive impairments. To date very few studies investigated social cognition in...
BACKGROUND
Schizophrenia and bipolar disorder are associated with neurocognitive and social-cognitive impairments. To date very few studies investigated social cognition in first-episode bipolar disorder (FEBD). Our main aim was to investigate the differences in social cognition and neurocognition between FEBD and first-episode psychosis (FEP). Another aim was to investigate neurocognitive correlates of negative symptoms and attenuated psychotic symptoms in FEBD.
METHODS
This study included 55 FEBD, 64 FEP and 43 healthy controls. A comprehensive neuropsychological battery assessing social cognition, processing speed, verbal and visual memory, working memory, sustained attention, and executive functions was administered to all participants.
RESULTS
Both FEBD and FEP were associated with widespread deficits in all neurocognitive domains and social cognition. Both FEP (d = -1.19) and FEBP (d = -0.88) were also impaired in social cognition. In FEP, effect sizes (Cohen's d) of neurocognitive deficits ranged from -0.71 to -1.56. FEBD was also associated with relatively milder but similar neurocognitive deficits (d = -0.61 to-1.17). FEBD group performed significantly better than FEP group in verbal and visual memory, processing speed, and executive function domains (d = -0.40 to-0.52). Negative symptoms and social functioning were associated with neuropsychological impairment in both groups. The severity of attenuated psychotic symptoms was associated with poorer verbal memory in FEBD (r = -0.39, p < 0.01).
LIMITATIONS
The cross-sectional nature of the current study is the main limitation.
CONCLUSIONS
Neurocognitive and social-cognitive deficits are evident in both FEBD and FEP. In FEBD, more severe memory deficits might be markers of clinical overlap and shared neurobiological vulnerability with psychotic disorders.
Topics: Humans; Bipolar Disorder; Cross-Sectional Studies; Social Cognition; Neuropsychological Tests; Psychotic Disorders; Memory, Short-Term; Memory Disorders; Cognition
PubMed: 38290586
DOI: 10.1016/j.jad.2024.01.237 -
Revue Neurologique 2017Temporal lobe epilepsy (TLE) is a type of epilepsy that often has a negative impact on patients' memory. Despite the importance of patients' complaints in this regard,... (Review)
Review
Temporal lobe epilepsy (TLE) is a type of epilepsy that often has a negative impact on patients' memory. Despite the importance of patients' complaints in this regard, the difficulties described by these patients are often not easy to demonstrate through a standard neuropsychological assessment. Accelerated long-term forgetting and autobiographical memory disorders are the two main memory impairments reported in the literature in patients with TLE. However, the methods used by different authors to evaluate long-term memory and autobiographical memory are heterogeneous. This heterogeneity can lead to differences in the observed results as well as how they are interpreted. Yet, despite the methodological differences, objectification of such memory deficits appears to be both specific and robust within this patient population. Analysis of the literature shows that accelerated long-term forgetting and autobiographical memory disorders share the same clinical characteristics. This leads to the assumption that they are, in fact, only one entity and that their evaluation may be done through a single procedure. Our proposal is to place this evaluation within the context of memory consolidation disorders. With such a perspective, evaluation of accelerated forgetting in autobiographical memory should consist of identifying a disorder in the formation and/or recovery of new memory traces.
Topics: Epilepsy, Temporal Lobe; Humans; Memory Disorders; Memory, Episodic; Memory, Long-Term; Neuropsychological Tests
PubMed: 28843413
DOI: 10.1016/j.neurol.2017.07.004 -
Biological Psychiatry Sep 2015For over a century, clinicians have consistently described the paradoxical co-existence in posttraumatic stress disorder (PTSD) of sensory intrusive hypermnesia and... (Review)
Review
For over a century, clinicians have consistently described the paradoxical co-existence in posttraumatic stress disorder (PTSD) of sensory intrusive hypermnesia and declarative amnesia for the same traumatic event. Although this amnesia is considered as a critical etiological factor of the development and/or persistence of PTSD, most current animal models in basic neuroscience have focused exclusively on the hypermnesia, i.e., the persistence of a strong fear memory, neglecting the qualitative alteration of fear memory. The latest is characterized by an underrepresentation of the trauma in the context-based declarative memory system in favor of its overrepresentation in a cue-based sensory/emotional memory system. Combining psychological and neurobiological data as well as theoretical hypotheses, this review supports the idea that contextual amnesia is at the core of PTSD and its persistence and that altered hippocampal-amygdalar interaction may contribute to such pathologic memory. In a first attempt to unveil the neurobiological alterations underlying PTSD-related hypermnesia/amnesia, we describe a recent animal model mimicking in mice some critical aspects of such abnormal fear memory. Finally, this line of argument emphasizes the pressing need for a systematic comparison between normal/adaptive versus abnormal/maladaptive fear memory to identify biomarkers of PTSD while distinguishing them from general stress-related, potentially adaptive, neurobiological alterations.
Topics: Animals; Disease Models, Animal; Fear; Humans; Memory Disorders; Mice; Stress Disorders, Post-Traumatic
PubMed: 26238378
DOI: 10.1016/j.biopsych.2015.06.017 -
Neuroscience and Biobehavioral Reviews Aug 2022The serotonergic system is involved in diverse cognitive functions including memory. Of particular importance to daily life are declarative memories that contain... (Review)
Review
The serotonergic system is involved in diverse cognitive functions including memory. Of particular importance to daily life are declarative memories that contain information about personal experiences, general facts, and events. Several psychiatric or neurological diseases, such as depression, attention-deficit-hyperactivity disorder (ADHD), and dementia, show alterations in serotonergic signalling and attendant memory disorders. Nevertheless, understanding serotonergic neurotransmission and its influence on memory remained a challenge until today. In this systematic review, we summarize recent psychopharmacological studies in animals and humans from a psychological memory perspective, in consideration of task-specific requirements. This approach has the advantage that comparisons between serotonin (5-HT)-related neurochemical mechanisms and manipulations are each addressing specific mnemonic circuits. We conclude that applications of the same 5-HT-related treatments can differentially affect unrelated tasks of declarative memories. Moreover, the analysis of specific mnemonic phases (e.g., encoding vs. consolidation) reveals opposing impacts of increased or decreased 5-HT tones, with low 5-HT supporting spatial encoding but impairing the consolidation of objects and verbal memories. Promising targets for protein synthesis-dependent consolidation enhancements include 5-HT receptor agonists and 5-HT receptor antagonists, with the latter being of special interest for the treatment of age-related decline. Further implications are pointed out as base for the development of novel therapeutic targets for memory impairment of neuropsychiatric disorders.
Topics: Animals; Attention Deficit Disorder with Hyperactivity; Cognition; Humans; Memory; Memory Disorders; Serotonin
PubMed: 35691469
DOI: 10.1016/j.neubiorev.2022.104729 -
Journal of Ethnopharmacology Oct 2022Yuanzhi Powder is a commonly used traditional Chinese medical formulae for its potency in enhancing memory and learning. In clinical practice, Yuanzhi Powder is a...
ETHNOPHARMACOLOGICAL RELEVANCE
Yuanzhi Powder is a commonly used traditional Chinese medical formulae for its potency in enhancing memory and learning. In clinical practice, Yuanzhi Powder is a classic formula in TCM to treat amnesia of the type "deficiency of Qi, turbid phlegm harasses the head and eyes, and stagnation of phlegm converting into the fire". Our previous study showed that Yuanzhi Power, used together with Codonopsis Radix (Dangshen Yuanzhi Power, DYP), could improve learning and memory ability in animals with memory disorder (MD) and its efficacy is superior or equivalent to that of the Yuanzhi Power.
AIM OF STUDY
This study aimed to explore the regulatory mechanism of DYP through the "bacteria-gut-brain axis".
MATERIALS AND METHODS
The SD rats were divided randomly into control, model, positive, DYP-L, and DYP-H groups. Except for the control group, the rats were intraperitoneally injected with D-Gal (400 mg/kg) and gavaged with aluminum chloride (200 mg/kg) every day for 50 days. The rats in the DYP group were gavaged with DYP (6.67 and 13.34 g/kg, respectively) from the 15th day, once a day. The rats in the positive group were similarly administrated with piracetam (0.5 g/kg). The rats' bodyweight was recorded from the 16th day. The learning and memory ability of animals was tested by Morris water maze. The levels of MCP-1, NF-L, NSE, and TNF-α in serum were determined by Elisa kit, while the histopathology of duodenum and colon tissues was examined by H & E staining. The diversity of intestinal flora was sequenced and analyzed. In order to reveal the role of intestinal flora in DYP treatment of MD, the intestinal flora composition and the correlation analysis of intestinal flora and the above biochemical indexes were investigated. The intestinal flora function and biological metabolic pathways were predicted and analyzed by the KEGG database.
RESULTS
The MD animals' learning and spatial memory ability decreased significantly, compared with the normal group, accompanied by weight increase and intestinal flora disorder. DYP can improve the learning and memory ability of MD animals, and its efficacy may exert through the following ways: (i) callback the abnormal biochemical indexes of MCP-1, NF-L, NSE, and TNF-α; (ii) decreasing the relative ratio of Firmicutes/Bacteroidetes and repairing the pathology of MD animal intestinal mucosa; and (iii) the regulation of DYP on biochemical blood indexes of MD animals was significantly correlated with the regulation of intestinal flora; (iv) DYP rats showed a strong correlation between cognitive ability improvement and bodyweight loss; (v) besides, DYP could also regulate the metabolic pathways of carbohydrate, amino acid, nucleotide, and energy by affecting related biological functions.
CONCLUSIONS
The results supported that DYP can improve MD animals' learning and memory ability by restoring the intestinal flora disorder and callback the abnormal biochemical indexes in serum, closely related to the "bacteria-gut-brain axis".
Topics: Animals; Codonopsis; Gastrointestinal Microbiome; Memory Disorders; Powders; Rats; Rats, Sprague-Dawley; Tumor Necrosis Factor-alpha
PubMed: 35640741
DOI: 10.1016/j.jep.2022.115410 -
Neural Plasticity 2015Major depressive disorder (MDD) is characterized by a dysfunctional processing of autobiographical memories. We review the following core domains of deficit: systematic... (Review)
Review
Major depressive disorder (MDD) is characterized by a dysfunctional processing of autobiographical memories. We review the following core domains of deficit: systematic biases favoring materials of negative emotional valence; diminished access and response to positive memories; a recollection of overgeneral memories in detriment of specific autobiographical memories; and the role of ruminative processes and avoidance when dealing with autobiographical memories. Furthermore, we review evidence from functional neuroimaging studies of neural circuits activated by the recollection of autobiographical memories in both healthy and depressive individuals. Disruptions in autobiographical memories predispose and portend onset and maintenance of depression. Thus, we discuss emerging therapeutics that target memory difficulties in those with depression. We review strategies for this clinical domain, including memory specificity training, method-of-loci, memory rescripting, and real-time fMRI neurofeedback training of amygdala activity in depression. We propose that the manipulation of the reconsolidation of autobiographical memories in depression might represent a novel yet largely unexplored, domain-specific, therapeutic opportunity for depression treatment.
Topics: Animals; Antidepressive Agents; Depressive Disorder; Humans; Memory Disorders; Memory, Episodic
PubMed: 26380121
DOI: 10.1155/2015/759139 -
Autism Research : Official Journal of... Feb 2024Individuals with autism spectrum disorder (ASD) frequently exhibit difficulties in retrieving autobiographical memories (AMs) of specific events from their life. Such... (Review)
Review
Individuals with autism spectrum disorder (ASD) frequently exhibit difficulties in retrieving autobiographical memories (AMs) of specific events from their life. Such memory deficits are frequently attributed to underlying disruptions in self-referential or social cognition processes. This makes intuitive sense as these are hallmarks of ASD. However, an emerging literature suggests that parallel deficits also exist in ASD individuals' ability to reconstruct the rich spatial contexts in which events occur. This is a capacity known as scene construction, and in typically developing individuals is considered a core process in retrieving AMs. In this review, we discuss evidence of difficulties with scene construction in ASD, drawing upon experiments that involve AM retrieval, other forms of mental time travel, and spatial navigation. We also highlight aspects of extant data that cannot be accounted for using purely social explanations of memory deficits in ASD. We conclude by identifying key questions raised by our framework and suggest how they might be addressed in future research.
Topics: Humans; Autism Spectrum Disorder; Memory, Episodic; Mental Recall; Memory Disorders; Spatial Navigation
PubMed: 38037250
DOI: 10.1002/aur.3066 -
Neurotoxicity Research Feb 2018Correlational and causal comparative research link ceramide (Cer), the precursor of complex sphingolipids, to some psychiatric (e.g., depression, schizophrenia (SZ),... (Review)
Review
Correlational and causal comparative research link ceramide (Cer), the precursor of complex sphingolipids, to some psychiatric (e.g., depression, schizophrenia (SZ), alcohol use disorder, and morphine antinociceptive tolerance) and neurological (e.g., Alzheimer's disease (AD), Parkinson disease (PD)) disorders. Cer generation can occur through the de novo synthesis pathway, the sphingomyelinase pathways, and the salvage pathway. The discoveries that plasma Cer concentration increase during depressive episodes in patients and that tricyclic and tetracyclic antidepressants functionally inhibit acid sphingomyelinase (ASM), the enzyme that catalyzes the degradation of sphingomyelin to Cer, have initiated a series of studies on the role of the ASM-Cer system in depressive disorder. Disturbances in the metabolism of Cer or SM are associated with the occurrence of SZ and PD. In both PD and SZ patients, the elevated levels of Cer or SM in the brain regions were associated with the disease. AD patients showed also an abnormal metabolism of brain Cer at early stages of the disease which may suggest Cer as an AD biomarker. In plasma of AD patients and in AD transgenic mice, ASM activity was increased. In contrast, partial ASM inhibition of Aβ deposition improved memory deficits. Furthermore, in clinical and preclinical research, ethanol enhanced activation of ASM followed by Cer production. Limited data have shown that Cer plays an important role in the development of morphine antinociceptive tolerance. In summary, clinical and preclinical findings provide evidence that targeting the Cer system should be considered as an innovative translational strategy for some brain disorders.
Topics: Alzheimer Disease; Antidepressive Agents; Brain; Ceramides; Memory Disorders; Sphingomyelin Phosphodiesterase
PubMed: 28842833
DOI: 10.1007/s12640-017-9798-6 -
Alzheimer's & Dementia : the Journal of... Jun 2020We explore here that memory loss observed in the early stage of Alzheimer's disease (AD) is a disorder of memory retrieval, instead of a storage impairment. This...
OBJECTIVE
We explore here that memory loss observed in the early stage of Alzheimer's disease (AD) is a disorder of memory retrieval, instead of a storage impairment. This engram-centric explanation aims to enlarge the conceptual frame of memory as an emergent behavior of the brain and to propose a new treatment strategy for memory retrieval in dementia-AD.
BACKGROUND
The conventional memory hypothesis suggests that memory is stored as multiple traces in hippocampal neurons but recent evidence indicates that there are specialized memory engrams responsible for the storage and the retrieval of different memory types.
UPDATED MEMORY HYPOTHESIS
There are specialized memory engram neurons for each memory type and when information will be stored as a memory arrives in the hippocampus through afferent neurons finds its neuron according to the excitability states of engram neurons. The excitability level in engram neurons seems like a code canalizing the interactions between engrams and information. Therefore, to enhance the excitability of memory engram neurons improves memory loss observed in AD. In addition, we suggest that the hippocampus creates an index for information stored in memory engram cells in specialized regions for different types of memory, instead of storing all information; and different anatomic locations of engram cells and their roles in memory retrieval point out that memory could be an emergent behavior of the brain, and the interaction between serotonin fluctuation and engram neurons could be neural underpinnings of terminal lucidity.
MAJOR CHALLENGES FOR THE MODEL
The major challenge for this engram-centric memory retrieval model is the translation from bench to patient, specifically the delivery of optogenetic tools in patients. Engram neurons can be specifically activated by optogenetic tools, but optogenetics is an invasive technique which requires optic fiber implantation into the brain. In addition, light can overheat the tissue and thus induce damage in tissue. Furthermore, light is a foreign object and its direct implantation into the brain may cause neuroinflammation, the main trigger of neurodegenerative diseases. Therefore, to test the engram hypothesis in human, new tools to allow specific engram activation should be discovered.
Topics: Animals; Brain; Humans; Memory; Memory Disorders; Models, Neurological; Neurons
PubMed: 32333509
DOI: 10.1002/alz.12071