Assessment of Memory Impairment in Early Diagnosis of Alzheimer’s Disease

2019 ◽  
Vol 16 (11) ◽  
pp. 975-985
Author(s):  
Martin Vyhnálek ◽  
Hana Marková ◽  
Jan Laczó ◽  
Rossana De Beni ◽  
Santo Di Nuovo
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Memory Impairment ◽  
Recent Progress ◽  
Memory Loss ◽  
Long Term Memory ◽  
Cognitive Changes ◽  
Memory Assessment ◽  
Memory Binding

Memory impairment has been considered as one of the earliest clinical hallmarks of Alzheimer’s disease. This paper summarizes recent progress in the assessment of memory impairment in predementia stages. New promising approaches of memory assessment include evaluation of longitudinal cognitive changes, assessment of long-term memory loss, evaluation of subjective cognitive concerns and testing of other memory modalities, such as spatial memory. In addition, we describe new challenging memory tests based on memory binding paradigms that have been recently developed and are currently being validated.

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

scholarly journals Noncanonical function of an autophagy protein prevents spontaneous Alzheimer’s disease

2020 ◽  
Vol 6 (33) ◽  
pp. eabb9036
Author(s):  
Bradlee L. Heckmann ◽  
Brett J. W. Teubner ◽  
Emilio Boada-Romero ◽  
Bart Tummers ◽  
Clifford Guy ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Human Disease ◽  
Memory Impairment ◽  
Memory Loss ◽  
Tau Hyperphosphorylation ◽  
Primary Microglia ◽  
Amyloid Aβ ◽  
Β Amyloid ◽  
Old Mice

Noncanonical functions of autophagy proteins have been implicated in neurodegenerative conditions, including Alzheimer’s disease (AD). The WD domain of the autophagy protein Atg16L is dispensable for canonical autophagy but required for its noncanonical functions. Two-year-old mice lacking this domain presented with robust β-amyloid (Aβ) pathology, tau hyperphosphorylation, reactive microgliosis, pervasive neurodegeneration, and severe behavioral and memory deficiencies, consistent with human disease. Mechanistically, we found this WD domain was required for the recycling of Aβ receptors in primary microglia. Pharmacologic suppression of neuroinflammation reversed established memory impairment and markers of disease pathology in this novel AD model. Therefore, loss of the Atg16L WD domain drives spontaneous AD in mice, and inhibition of neuroinflammation is a potential therapeutic approach for treating neurodegeneration and memory loss. A decline in expression of ATG16L in the brains of human patients with AD suggests the possibility that a similar mechanism may contribute in human disease.

scholarly journals On the relationship between knowledge and memory for pictures: Evidence from the study of patients with semantic dementia and Alzheimer's disease

1997 ◽  
Vol 3 (6) ◽  
pp. 534-544 ◽  
Author(s):  
KIM S. GRAHAM ◽  
JAMES T. BECKER ◽  
JOHN R. HODGES
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Medial Temporal Lobe ◽  
Semantic Dementia ◽  
Long Term Memory ◽  
New Learning ◽  
The Relationship ◽  
Hippocampal Complex ◽  
Temporal Neocortex

Current views of long-term memory presume that both the hippocampal complex and the neocortex play interactive, but separate, roles in the storage of memories. While the neocortex is considered the eventual and permanent store for our memories, the encoding of recently experienced events is thought to be initially dependent upon the hippocampus and closely related structures. Neuropsychological studies have demonstrated that damage to the medial temporal lobe results in a retrograde amnesia extending back in time, with better preservation of older memories. The converse pattern has been shown in patients with semantic dementia, who have focal atrophy of the inferolateral temporal neocortex, but relative sparing of the hippocampal complex (Graham & Hodges, 1997). Here we demonstrate that such patients can show relatively preserved new learning on a forced-choice recognition memory test (based on real and chimeric animals), while patients in the early amnestic phase of Alzheimer's disease show severely impaired learning on the same test. This result provides support for the view that new learning is primarily dependent upon the hippocampus and related structures. (JINS, 1997, 3, 534–544.)

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 Liraglutide Protects Against Brain Amyloid-β1–42 Accumulation in Female Mice with Early Alzheimer’s Disease-Like Pathology by Partially Rescuing Oxidative/Nitrosative Stress and Inflammation

2020 ◽  
Vol 21 (5) ◽  
pp. 1746 ◽  
Author(s):  
Ana I. Duarte ◽  
Emanuel Candeias ◽  
Inês N. Alves ◽  
Débora Mena ◽  
Daniela F. Silva ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Nitrosative Stress ◽  
Senile Plaques ◽  
Memory Loss ◽  
Mature Female ◽  
Cognitive Changes ◽  
Female Mice ◽  
Early Alzheimer’S Disease

Alzheimer’s disease (AD) is the most common form of dementia worldwide, being characterized by the deposition of senile plaques, neurofibrillary tangles (enriched in the amyloid beta (Aβ) peptide and hyperphosphorylated tau (p-tau), respectively) and memory loss. Aging, type 2 diabetes (T2D) and female sex (especially after menopause) are risk factors for AD, but their crosslinking mechanisms remain unclear. Most clinical trials targeting AD neuropathology failed and it remains incurable. However, evidence suggests that effective anti-T2D drugs, such as the GLP-1 mimetic and neuroprotector liraglutide, can be also efficient against AD. Thus, we aimed to study the benefits of a peripheral liraglutide treatment in AD female mice. We used blood and brain cortical lysates from 10-month-old 3xTg-AD female mice, treated for 28 days with liraglutide (0.2 mg/kg, once/day) to evaluate parameters affected in AD (e.g., Aβ and p-tau, motor and cognitive function, glucose metabolism, inflammation and oxidative/nitrosative stress). Despite the limited signs of cognitive changes in mature female mice, liraglutide only reduced their cortical Aβ1–42 levels. Liraglutide partially attenuated brain estradiol and GLP-1 and activated PKA levels, oxidative/nitrosative stress and inflammation in these AD female mice. Our results support the earlier use of liraglutide as a potential preventive/therapeutic agent against the accumulation of the first neuropathological features of AD in females.

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