Association of subjective memory complaint and depressive symptoms with objective cognitive functions in prodromal Alzheimer's disease including pre-mild cognitive impairment

2017 ◽  
Vol 217 ◽  
pp. 24-28 ◽  
Author(s):  
Eun Hyun Seo ◽  
Hoowon Kim ◽  
Kyu Yeong Choi ◽  
Kun Ho Lee ◽  
IL Han Choo
2017 ◽  
Vol 29 (9) ◽  
pp. 1543-1550 ◽  
Author(s):  
Mehmet Yuruyen ◽  
Gozde Gultekin ◽  
Gizem Cetiner Batun ◽  
Hakan Yavuzer ◽  
Fundan Engin Akcan ◽  
...  

ABSTRACTBackground:Alteration in energy expenditure or metabolism is the most accused risk issue for the onset and for the course of neurodegenerative cognitive disorders. Neuropeptides are suggested to be related with learning and memory. Phoenixin (PNX) is the most recently reported neuropeptide and we aimed to compare the plasma level in people with subjective memory complaints, patients with mild cognitive impairment, and mild Alzheimer's disease (AD).Methods:Ninety two participants enrolled in the study. After screening tests, all participants were assessed with a neuropsychological battery for further cognitive evaluations. We used ELISA kit to assay the level of Human PNX.Results:Patients with AD were significantly older than people in subjective memory complaint group (p = 0.02). There was no significant difference between groups according to gender (p = 0.435). Mean plasma PNX level was not significantly different between groups (p = 0.279). Mean plasma PNX level in MCI group was positively correlated with BMI (r = 0.402 and p = 0.028), serum HDL level (r = 0.454 and p = 0.012), blood systolic pressure (r = 0.428 and p = 0.018) and negatively correlated with logical memory (r=−0.335 and p=0.031). The mean plasma PNX level was positively correlated with immediate recall in subjective memory complaint group (r = 0.417 and p = 0.034).Conclusion:This study is the first studying the association of plasma PNX level and cognitive complaints or decline. The knowledge about the role, interaction, and physiological functions of PNX is lacking. Lower plasma PNX level might be important in prodromal stages as MCI and the predictive role of PNX should be investigated in further studies.


2020 ◽  
Vol 2 (2) ◽  
Author(s):  
Jiangyi Xia ◽  
Ali Mazaheri ◽  
Katrien Segaert ◽  
David P Salmon ◽  
Danielle Harvey ◽  
...  

Abstract Reliable biomarkers of memory decline are critical for the early detection of Alzheimer’s disease. Previous work has found three EEG measures, namely the event-related brain potential P600, suppression of oscillatory activity in the alpha frequency range (∼10 Hz) and cross-frequency coupling between low theta/high delta and alpha/beta activity, each of which correlates strongly with verbal learning and memory abilities in healthy elderly and patients with mild cognitive impairment or prodromal Alzheimer’s disease. In the present study, we address the question of whether event-related or oscillatory measures, or a combination thereof, best predict the decline of verbal memory in mild cognitive impairment and Alzheimer’s disease. Single-trial correlation analyses show that despite a similarity in their time courses and sensitivities to word repetition, the P600 and the alpha suppression components are minimally correlated with each other on a trial-by-trial basis (generally |rs| < 0.10). This suggests that they are unlikely to stem from the same neural mechanism. Furthermore, event-related brain potentials constructed from bandpass filtered (delta, theta, alpha, beta or gamma bands) single-trial data indicate that only delta band activity (1–4 Hz) is strongly correlated (r = 0.94, P < 0.001) with the canonical P600 repetition effect; event-related potentials in higher frequency bands are not. Importantly, stepwise multiple regression analyses reveal that the three event-related brain potential/oscillatory measures are complementary in predicting California Verbal Learning Test scores (overall R2’s in 0.45–0.63 range). The present study highlights the importance of combining EEG event-related potential and oscillatory measures to better characterize the multiple mechanisms of memory failure in individuals with mild cognitive impairment or prodromal Alzheimer’s disease.


2016 ◽  
Vol 10 (3) ◽  
pp. 170-177 ◽  
Author(s):  
Adalberto Studart Neto ◽  
Ricardo Nitrini

ABSTRACT Background: Mild cognitive impairment is considered as the first clinical manifestation of Alzheimer's disease (AD), when the individual exhibits below performance on standardized neuropsychological tests. However, some subjects before having a lower performance on cognitive assessments already have a subjective memory complaint. Objective: A review about subjective cognitive decline, the association with AD biomarkers and risk of conversion to dementia. Methods: We performed a comprehensive non-systematic review on PubMed. The keywords used in the search were terms related to subjective cognitive decline. Results: Subjective cognitive decline is characterized by self-experience of deterioration in cognitive performance not detected objectively through formal neuropsychological testing. However, various terms and definitions have been used in the literature and the lack of a widely accepted concept hampers comparison of studies. Epidemiological data have shown that individuals with subjective cognitive decline are at increased risk of progression to AD dementia. In addition, there is evidence that this group has a higher prevalence of positive biomarkers for amyloidosis and neurodegeneration. However, Alzheimer's disease is not the only cause of subjective cognitive decline and various other conditions can be associated with subjective memory complaints, such as psychiatric disorders or normal aging. The features suggestive of a neurodegenerative disorder are: onset of decline within the last five years, age at onset above 60 years, associated concerns about decline and confirmation by an informant. Conclusion: These findings support the idea that subjective cognitive complaints may be an early clinical marker that precedes mild cognitive impairment due to Alzheimer's disease.


Sign in / Sign up

Export Citation Format

Share Document