The andropause and memory loss: is there a link between androgen decline and dementia in the aging male?

Studies demonstrate a decline in androgens with age and this results in the andropause. The objective of this paperis to review the literature on hormonal changes that occur in the aging males and determine if there are associations be-tween decreased testosterone, dehydroepiandrosterone (DHEA) and decreased cognitive function. Trials of androgen re-placement and its impact on cognitive function will also be analyzed. Method of analysis will be by a thorough searchof articles on MEDLINE, the Internet and major abstract databases. Results of the author's own research in 302 men ofthe association of memory loss as a symptom in the andropause will be presented. In addition, the authors open trial oftestosterone replacement in hypogonadic men with Alzheimer's disease will also be presented. The results of the author'strial will be compared with other investigators. High endogenous testosterone level predicted better performance on visu-al spatial tests in several studies, but not in all studies. Likewise, testosterone replacement in hypogonadic patients im-proved cognitive functions in some but not all studies. Testosterone has also been shown to improve cognitive functionin eugonadal men. Several studies have shown that declines in DHEA may contribute to Alzheimer's disease and the re-sults of double blind studies with DHEA replacement and its effect on cognition will also be presented. In summary,there is still no consensus that androgen replacement is beneficial in cognitive decline but this option may prove promis-ing in some patients. (Asian J Androl 2001 Sep; 3: 169-174)

Rarely fast progressive memory loss diagnosed as Creutzfeldt-Jakob disease:A case report

BACKGROUND Creutzfeldt-Jakob disease(CJD)is a rare degenerative disease of the central nervous system that can be contagious or hereditary and is a rare cause of rapidly progressive dementia.It almost always results in death within 1-2 years from symptom onset.CASE SUMMARY Here,we report the case of a 57-year-old male who initially experienced dizziness followed by a 1-mo fast decline in memory function.He presented to the local hospital and underwent magnetic resonance imaging and cerebrospinal fluid(CSF)examination,with no definitive diagnosis.However,the symptoms of progressive forgetting worsened.In addition,he exhibited progressive involuntary tremor of the limbs.Then,he came to our hospital,and according to the results of CSF examination,electroencephalography(EEG)and magnetic resonance imaging(MRI)tests and clinical manifestations of cerebellar ataxia,dementia,and myoclonus that rapidly progressed,with a short duration of illness,he was finally diagnosed with sporadic CJD(sCJD).CONCLUSION This case report aims to create awareness among physicians to emphasize auxiliary examination,CSF examination,EEG and MRI tests and recognition of cerebellar ataxia,dementia,and myoclonus that rapidly progress to prompt pursuit of an early diagnosis and identification of sCJD and to reduce complications.

Prediction of Attention and Short-Term Memory Loss by EEG Workload Estimation

Mental workload plays a vital role in cognitive impairment. The impairment refers to a person’s difficulty in remembering, receiving new information, learning new things, concentrating, or making decisions that seriously affect everyday life. In this paper, the simultaneous capacity (SIMKAP) experiment-based EEG workload analysis was presented using 45 subjects for multitasking mental workload estimation with subject wise attention loss calculation as well as short term memory loss measurement. Using an open access preprocessed EEG dataset, Discrete wavelet transforms (DWT) was utilized for feature extraction and Minimum redundancy and maximum relevancy (MRMR) technique was used to select most relevance features. Wavelet decomposition technique was also used for decomposing EEG signals into five sub bands. Fourteen statistical features were calculated from each sub band signal to form a 5 × 14 window size. The Neural Network (Narrow) classification algorithm was used to classify dataset for low and high workload conditions and comparison was made using some other machine learning models. The results show the classifier’s accuracy of 86.7%, precision of 84.4%, F1 score of 86.33%, and recall of 88.37% that crosses the state-of-the art methodologies in the literature. This prediction is expected to greatly facilitate the improved way in memory and attention loss impairments assessment.

Therapeutic potential of Carum carvi in depression,memory loss,and hippocampal sclerosis reversal in temporal lobe epilepsy

Background:Epilepsy is a disease characterized by unprovoked seizures,and it affects around 70 million people worldwide.Standard treatment is ineffective in one third of all epilepsy patients.Temporal Lobe Epilepsy with Hippocampal Sclerosis(TLE-HS)is the most drug-resistant form of epilepsy,and it also impacts physical,mental,and psychological well-being of patients.Carum carvi extract has demonstrated anti-convulsant,anti-depressant,and anxiolytic properties.This study was designed to investigate if Carum carvi extract can alleviate depression and memory loss symptoms in a TLE-HS animal model.Methods:Male Sprague Dawley rats were used to create a model of TLE-HS and Carum carvi extract treatment,along with appropriate controls,was used to test the efficacy of this herbal extract in reducing the symptoms of depression and memory loss.Results:Forced swim test showed that Carum carvi extract treated TLE-HS rats resulted in significant improvement of the symptoms of depression.However,novel object recognition test showed that memory improvement did not occur.Conclusion:Depression significantly impacts the quality of life in TLE-HS patients,and this study has shown that Carum carvi extract should be explored further as an adjuvant treatment for TLE-HS patients to improve their quality of life.

Promotion of structural plasticity in area V2 of visual cortex prevents against object recognition memory deficits in aging and Alzheimer's disease rodents

Memory deficit,which is often associated with aging and many psychiatric,neurological,and neurodegenerative diseases,has been a challenging issue for treatment.Up till now,all potential drug candidates have failed to produce satisfa ctory effects.Therefore,in the search for a solution,we found that a treatment with the gene corresponding to the RGS14414protein in visual area V2,a brain area connected with brain circuits of the ventral stream and the medial temporal lobe,which is crucial for object recognition memory(ORM),can induce enhancement of ORM.In this study,we demonstrated that the same treatment with RGS14414in visual area V2,which is relatively unaffected in neurodegenerative diseases such as Alzheimer s disease,produced longlasting enhancement of ORM in young animals and prevent ORM deficits in rodent models of aging and Alzheimer’s disease.Furthermore,we found that the prevention of memory deficits was mediated through the upregulation of neuronal arbo rization and spine density,as well as an increase in brain-derived neurotrophic factor(BDNF).A knockdown of BDNF gene in RGS14414-treated aging rats and Alzheimer s disease model mice caused complete loss in the upregulation of neuronal structural plasticity and in the prevention of ORM deficits.These findings suggest that BDNF-mediated neuronal structural plasticity in area V2 is crucial in the prevention of memory deficits in RGS14414-treated rodent models of aging and Alzheimer’s disease.Therefore,our findings of RGS14414gene-mediated activation of neuronal circuits in visual area V2 have therapeutic relevance in the treatment of memory deficits.

Loss of canonical Wnt signaling is involved in the pathogenesis of Alzheimer's disease

Alzheimer＇s disease（AD） is the most common form of dementia in the older population, however, the precise cause of the disease is unknown. The neuropathology is characterized by the presence of aggregates formed by amyloid-β（Aβ） peptide and phosphorylated tau; which is accompanied by progressive impairment of memory. Diverse signaling pathways are linked to AD, and among these the Wnt signaling pathway is becoming increasingly relevant, since it plays essential roles in the adult brain. Initially, Wnt signaling activation was proposed as a neuroprotective mechanism against Aβ toxicity. Later, it was reported that it participates in tau phosphorylation and processes of learning and memory. Interestingly, in the last years we demonstrated that Wnt signaling is fundamental in amyloid precursor protein（APP） processing and that Wnt dysfunction results in Aβ production and aggregation in vitro. Recent in vivo studies reported that loss of canonical Wnt signaling exacerbates amyloid deposition in a transgenic（Tg） mouse model of AD. Finally, we showed that inhibition of Wnt signaling in a Tg mouse previously at the appearance of AD signs, resulted in memory loss, tau phosphorylation and Aβ formation and aggregation; indicating that Wnt dysfunction accelerated the onset of AD. More importantly, Wnt signaling loss promoted cognitive impairment, tau phosphorylation and Aβ1–42 production in the hippocampus of wild-type（WT） mice, contributing to the development of an Alzheimer＇s-like neurophatology. Therefore, in this review we highlight the importance of Wnt/β-catenin signaling dysfunction in the onset of AD and propose that the loss of canonical Wnt signaling is a triggering factor of AD.

“Life, Memory, Recognition and Aging” of Grey Tin

It was shown that tin has two types of memory: 1) “memory of the structure” about of the event when it was in the α configuration, and 2) “memory of recognition (discern)” whereby tin recognises that an object with which it in contact, was previously in contact with substances of a particular type (“infection”). Transformations of metallic white tin into the grey semiconductor occur with the help of either small pieces of grey tin or other substances isomorphous with grey tin [1] [2] [3]. These pieces (when pressed into white tin) initiate phase transition (by “infection”) from white tin into grey tin. Once the tin is transformed into its grey form, it retains a “memory” about this after it is transferred back into white tin. Thus, for second and subsequent phase transformations, there is no need for external initiators to be used. The tin has the “memory of recognition” too—when the tin can recognises that an object with which it is in contact, was previously in contact with the “infection”. This phenomenon is concerned with the aging of tin: firstly, with the loss of “memory of the structure” of tin of the event when it was in the grey tin configuration, and, secondly, with the loss of “memory of recognition” of tin whereby the tin recognises that an object with which it is in contact, was previously in contact with substances of a particular type. Factors that effect the aging of tin has been studied in detail and an explanation of the mechanism of action of these factors has been suggested.

Stem cell therapy for Alzheimer’s disease:An overview of experimental models and reality

Alzheimer's disease(AD)is a neurodegenerative disorder.The pathology of AD is characterized by extracellular amyloid beta(Aβ)plaques,neurofibrillary tangles com-posed of hyperphosphorylated tau,neuronal death,synapse loss,and brain atrophy.Many therapies have been tested to improve or at least effectively modify the course of AD.Meaningful data indicate that the transplantation of stem cells can alleviate neuropathology and significantly ameliorate cognitive deficits in animal models with Alzheimer's disease.Transplanted stem cells have shown their inherent advantages in improving cognitive impairment and memory dysfunction,although certain weak-nesses or limitations need to be overcome.This review recapitulates rodent models for AD,the therapeutic efficacy of stem cells,influencing factors,and the underlying mechanisms behind these changes.Stem cell therapy provides perspective and chal-lenges for its clinical application in the future.

Effectiveness of lorazepam-assisted interviews in an adolescent with dissociative amnesia A case report

To facilitate gathering information during a psychiatric interview, some psychiatrists advocate augmenting the interview using drugs. Rather than barbiturates, benzodiazepines have been used for drug-assisted interviews. Dissociative amnesia is one of the indications for these interviews. Herein, we present the case of a 15-year-old female who was diagnosed as having dissociative amnesia because of conflicts with her friends. She was administered a Iorazepam-assisted interview to aid recovery of her memories. In this case, a small dose of Iorazepam was sufficient to recover her memories without any adverse effects.

Transplantation of bone marrow mesenchymal stem cells improves cognitive deficits and alleviates neuropathology in animal models of Alzheimer’s disease: a meta-analytic review on potential mechanisms

Background Alzheimer’s disease is a neurodegenerative disorder.Therapeutically,a transplantation of bone marrow mesenchymal stem cells(BMMSCs)can play a beneficial role in animal models of Alzheimer’s disease.However,the relevant mechanism remains to be fully elucidated.Main body Subsequent to the transplantation of BMMSCs,memory loss and cognitive impairment were significantly improved in animal models with Alzheimer’s disease(AD).Potential mechanisms involved neurogenesis,apoptosis,angiogenesis,inflammation,immunomodulation,etc.The above mechanisms might play different roles at certain stages.It was revealed that the transplantation of BMMSCs could alter some gene levels.Moreover,the differential expression of representative genes was responsible for neuropathological phenotypes in Alzheimer’s disease,which could be used to construct gene-specific patterns.Conclusions Multiple signal pathways involve therapeutic mechanisms by which the transplantation of BMMSCs improves cognitive and behavioral deficits in AD models.Gene expression profile can be utilized to establish statistical regression model for the evaluation of therapeutic effect.The transplantation of autologous BMMSCs maybe a prospective therapy for patients with Alzheimer’s disease.