Cerebral dopamine neurotrophic factor improves long-term memory in APP/PS1 transgenic mice modeling Alzheimer's disease as well as in wild-type mice

2015 ◽  
Vol 291 ◽  
pp. 1-11 ◽  
Author(s):  
Susanna Kemppainen ◽  
Päivi Lindholm ◽  
Emilia Galli ◽  
Hanna-Maija Lahtinen ◽  
Henna Koivisto ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transgenic Mice ◽  
Neurotrophic Factor ◽  
Long Term Memory ◽  
Wild Type ◽  
Term Memory ◽  
Cerebral Dopamine Neurotrophic Factor ◽  
Cerebral Dopamine

scholarly journals Disruption of the astrocyte–neuron interaction is responsible for the impairments in learning and memory in 5XFAD mice: an Alzheimer’s disease animal model

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Moonseok Choi ◽  
Sang-Min Lee ◽  
Dongsoo Kim ◽  
Heh-In Im ◽  
Hye-Sun Kim ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Animal Model ◽  
Memory Formation ◽  
Long Term Memory ◽  
Term Memory ◽  
Stat3 Phosphorylation ◽  
Neuron Interactions ◽  
5Xfad Mice

AbstractThe morphological dynamics of astrocytes are altered in the hippocampus during memory induction. Astrocyte–neuron interactions on synapses are called tripartite synapses. These control the synaptic function in the central nervous system. Astrocytes are activated in a reactive state by STAT3 phosphorylation in 5XFAD mice, an Alzheimer’s disease (AD) animal model. However, changes in astrocyte–neuron interactions in reactive or resting-state astrocytes during memory induction remain to be defined. Here, we investigated the time-dependent changes in astrocyte morphology and the number of astrocyte–neuron interactions in the hippocampus over the course of long-term memory formation in 5XFAD mice. Hippocampal-dependent long-term memory was induced using a contextual fear conditioning test in 5XFAD mice. The number of astrocytic processes increased in both wild-type and 5XFAD mice during memory formation. To assess astrocyte–neuron interactions in the hippocampal dentate gyrus, we counted the colocalization of glial fibrillary acidic protein and postsynaptic density protein 95 via immunofluorescence. Both groups revealed an increase in astrocyte–neuron interactions after memory induction. At 24 h after memory formation, the number of tripartite synapses returned to baseline levels in both groups. However, the total number of astrocyte–neuron interactions was significantly decreased in 5XFAD mice. Administration of Stattic, a STAT3 phosphorylation inhibitor, rescued the number of astrocyte–neuron interactions in 5XFAD mice. In conclusion, we suggest that a decreased number of astrocyte–neuron interactions may underlie memory impairment in the early stages of AD.

Regulation of aberrant proteasome activity re‐establishes plasticity and long‐term memory in an animal model of Alzheimer's disease

2020 ◽  
Vol 34 (7) ◽  
pp. 9466-9479
Author(s):  
Kumar Krishna‐K ◽  
Nimmi Baby ◽  
Radha Raghuraman ◽  
Sheeja Navakkode ◽  
Thomas Behnisch ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Animal Model ◽  
Proteasome Activity ◽  
Long Term Memory ◽  
Term Memory ◽  
Model Of Alzheimer’S Disease

Short- and long-term memory in patients with presenile dementia (Alzheimer's disease)

1973 ◽  
Vol 3 (2) ◽  
pp. 221-224 ◽  
Author(s):  
Edgar Miller
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Short Term Memory ◽  
Long Term Memory ◽  
Hippocampal Damage ◽  
Presenile Dementia ◽  
Term Memory ◽  
Memory Disorder ◽  
Long Term Storage

SynopsisEvidence is presented to show that patients with Alzheimer's disease owe their memory disturbance to both an impairment in short-term memory and an additional difficulty in establishing new material in long-term storage. These findings are particularly discussed in relation to the notion that, since the pathological changes in Alzheimer's disease are particularly manifest in the hippocampal region, then this involvement of the hippocampus might explain the memory disorder. The present experiment, which is similar to one previously reported using subjects with bilateral hippocampal lesions, shows the two types of memory disorder resulting from bilateral hippocampal damage and Alzheimer's disease to be qualitatively different. Some outstanding problems with regard to obtaining a complete understanding of the nature of the amnesic phenomena in Alzheimer's disease are discussed.

scholarly journals Distinct Effects of The Hippocampal Transplantation of Neural And Mesenchymal Stem Cell In a Transgenic Model of Alzheimer’s Disease

2021 ◽  
Author(s):  
Henrique Correia Campos ◽  
Deidiane Elisa Ribeiro ◽  
Debora Hashiguchi ◽  
Deborah Hukuda ◽  
Christiane Gimenes ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Stem Cells ◽  
Amyloid Β ◽  
Microglia Activation ◽  
Long Term Memory ◽  
Object Recognition Test ◽  
Term Memory ◽  
Model Of Alzheimer’S Disease

Abstract Alzheimer’s disease (AD) is a highly disabling condition, with no cure currently available that accounts for 60-70% of all dementia cases worldwide. Therefore, the study of possible therapeutic strategies for AD is required. For that, animal models which resemble the main aspects of AD has been largely employed. Similar to AD patients, the double transgenic APPswe/PS1dE9 (APP/PS1) mice presents amyloid-β (Αβ) plaques in the cortex and hippocampus, hyperlocomotion, cognitive deficits, and exacerbated inflammatory response. Recent studies showed that these neuropathological features were reversed by the transplantation of stem cells. However, the comparison of the effects induced by neural (NSC) or mesenchymal (MSC) stem cells was never investigated in an AD animal model before. In view of that, the present study aimed to evaluate whether NSC or MSC transplantation into the hippocampus of APP/PS1 mice reverse AD-related alterations, namely locomotor activity (open field test), short- and long-term memory (object recognition test), Αβ plaques formation (6-E10 immune staining) and microglia activation (Iba-1 immune staining) in the hippocampus. NSC and MSC engraftment reduced the number of hippocampal Αβ plaques in the hippocampus of APP/PS1 mice, and NSC reverted the peripheral hyperlocomotion activity displayed by APP/PS1 mice. Surprisingly, NSC increased microglia activation in the hippocampus of APP/PS1 mice and no impairment in short or long-term memory was observed in APP/PS1 mice. Altogether, this study reinforces the possible beneficial effects of NSC or MSC transplantation in the AD treatment.

scholarly journals Behavioral Improvements and its Molecular Mechanism of Ilex kudingcha C.J. Tseng on Animal Model of Alzheimer’s Disease

2020 ◽  
Vol 25 (3) ◽  
Author(s):  
Lap Thi Nguyen ◽  
Nguyen Huu Son ◽  
Tran Nguyen Hong ◽  
Nguyen Minh Khoi ◽  
Kinzo Matsumoto ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Muscarinic Receptor ◽  
Short Term Memory ◽  
Long Term Memory ◽  
Short Term ◽  
Reference Drug ◽  
Term Memory ◽  
Model Of Alzheimer’S Disease

Alzheimer's disease (AD) is a common chronic neurodegenerative disease with well-defined pathophysiological mechanisms. Ilex kudingcha (IK) C.J. Tseng is commonly known as bitter tea or “Khom” tea in Vietnam. The present study was conducted to investigate the anti-dementia effect of IK using olfactory bulbectomized (OBX) mice. OBX mice were daily treated with IK extract (540 mg/kg) or reference drug, tacrine (2.5 mg/kg) 1 week before and continuously for 3 days after the OBX surgery. The object recognition test, modified Y maze test and fear conditioning test were employed to analyze non-spatial short-term, spatial short-term and long-term memories of the mice respectively. Administration of IK extract and tacrine attenuated these OBX-induced cognitive deficits in mice. The effects of IK and tacrine on spatial short-term memory impairment were reversed by scopolamine, a muscarinic receptor antagonist. The amyloid-beta (Aβ) production in adult transgenic Drosophila brain flies was also investigated by using Western blotting with APP-HA antibody. These results indicated that IK extract improves short-term and long-term memory disturbances in OBX mice and that muscarinic receptor may play a role on these actions. In addition, our result also showed that IK extract reduces the expression of amyloid precursor protein (APP) in brain of AD model using Drosophila melanogaster.

scholarly journals Galantamine plasma concentration and cognitive response in Alzheimer’s disease

PeerJ ◽  
2019 ◽  
Vol 7 ◽  
pp. e6887 ◽  
Author(s):  
Yi-Ting Lin ◽  
Mei-Chuan Chou ◽  
Shyh-Jong Wu ◽  
Yuan-Han Yang
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Plasma Concentration ◽  
Plasma Concentrations ◽  
Cognitive Domain ◽  
Long Term Memory ◽  
Cognitive Responses ◽  
Cognitive Response ◽  
Term Memory

Background Galantamine has been approved for the treatment of Alzheimer’s disease (AD). However, there are few studies which have reported the association between cognitive responses and galantamine plasma concentration. The aim of this study was to determine the correlation between galantamine plasma concentration and the subsequent cognitive response following treatment in AD patients. Methods AD sufferers who continuously took 8 mg/d galantamine for at least 6 months without previous exposure to other kinds of AChEI such as donepezil, rivastigmine, or memantine were included in this cohort study. The assessments included the Mini Mental Status Examination (MMSE), Clinical Dementia Rating Scale (CDR) and the Cognitive Assessment Screening Instrument (CASI). Each subdomain of the CASI assessment was conducted at baseline and after 6 months of galantamine. The plasma concentrations of galantamine were measured by capillary electrophoresis after 6 months of the treatment. Logistic regression was performed to adjust for age, gender, apolipoprotein E ε4 genotype status, and baseline score to investigate the association between galantamine plasma concentrations and the cognitive response. Results The total sample consisted of 33 clinically diagnosed AD patients taking galantamine 8 mg/d for 6 months. There was no linear correlation between galantamine concentration and cognitive response in patients. However, 22 patients were responsive to the treatment in the long-term memory domain. In CASI subset domain, concentration improved during the 6 months follow up. Conclusions In the limited samples study, galantamine mostly benefitted the cognitive domain of long-term memory. The benefits were not related to the galantamine plasma concentration. Objective intra-individual evaluation of therapeutic response should be encouraged.

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