Amygdalar Atrophy in Early Alzheimer’s Disease

Klein-Koerkamp, Yanica; Heckemann, Rolf A.; Ramdeen, Kylee T.; Moreaud, Olivier; Keignart, S.; Krainik, Alexandre; Hammers, Alexander; Baciu, Monica; Hot, Pascal; Initiative, for the Disease Neuroimaging

doi:10.2174/1567205011666140131123653

Cited by 50 publications

(29 citation statements)

References 79 publications

(154 reference statements)

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“…However, NAR pre-treatment significantly protected rat recognition memory possibly by protecting cortical neurodegeneration produced by AlCl 3 and D-gal. Regions that are mainly affected in AD brain are cortex, hippocampus, and amygdala [51,52]. We found that in AD-like model rat's associative memory was severely impaired whereas NAR protected rat's associative memory in AlCl 3 +D-gal induced cognitive deficits in PAT.…”

Section: Discussionmentioning

confidence: 73%

Naringenin protects AlCl3/D-galactose induced neurotoxicity in rat model of AD via attenuation of acetylcholinesterase levels and inhibition of oxidative stress

et al. 2020

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Currently prescribed medications for the treatment of Alzheimer's disease (AD) that are based on acetylcholinesterase inhibition only offer symptomatic relief but do not provide protection against neurodegeneration. There appear to be an intense need for the development of therapeutic strategies that not only improve brain functions but also prevent neurodegeneration. The oxidative stress is one of the main causative factors of AD. Various antioxidants are being investigated to prevent neurodegeneration in AD. The objective of this study was to investigate the neuroprotective effects of naringenin (NAR) against AlCl 3 +D-gal induced AD-like symptoms in an animal model. Rats were orally pre-treated with NAR (50 mg/kg) for two weeks and then exposed to AlCl 3 +D-gal (150 mg/kg + 300 mg/kg) intraperitoneally for one week to develop AD-like symptoms. The standard drug, donepezil (DPZ) was used as a stimulator of cholinergic activity. Our results showed that NAR pre-treatment significantly protected AD-like behavioral disturbances in rats. In DPZ group, rats showed improved cognitive and cholinergic functions but the neuropsychiatric functions were not completely improved and showed marked histopathological alterations. However, NAR not only prevented AlCl 3 +D-gal induced AD-like symptoms but also significantly prevented neuropsychiatric dysfunctions in rats. Results of present study suggest that NAR may play a role in enhancing neuroprotective and cognition functions and it can potentially be considered as a neuroprotective compound for therapeutic management of AD in the future. PLOS ONE | https://doi.org/10.1371/journal.pone.0227631 January 16, 2020 1 / 30 OPEN ACCESS Citation: Haider S, Liaquat L, Ahmad S, Batool Z, Siddiqui RA, Tabassum S, et al. (2020) Naringenin protects AlCl 3 /D-galactose induced neurotoxicity in rat model of AD via attenuation of acetylcholinesterase levels and inhibition of oxidative stress. PLoS ONE 15(1): e0227631.

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Section: Discussionmentioning

confidence: 73%

Naringenin protects AlCl3/D-galactose induced neurotoxicity in rat model of AD via attenuation of acetylcholinesterase levels and inhibition of oxidative stress

et al. 2020

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“…Amygdala volume is significantly reduced in AD in a similar magnitude to the hippocampus (Klein-Koerkamp et al, 2014). However, we have previously shown that amygdala atrophy is not identified over a 2 year follow-up period in elderly population samples, which contrasts with significant atrophy in the hippocampus (Jiang et al, 2014a).…”

Section: Discussionmentioning

confidence: 99%

The effect of increased genetic risk for Alzheimer's disease on hippocampal and amygdala volume

Lupton

Strike

Hansell

et al. 2016

Neurobiology of Aging

109

107

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Reduction in hippocampal and amygdala volume measured via structural magnetic resonance imaging is an early marker of Alzheimer’s disease (AD). Whether genetic risk factors for AD exert an effect on these subcortical structures independent of clinical status has not been fully investigated. We examine whether increased genetic risk for AD influences hippocampal and amygdala volumes in case-control and population cohorts at different ages, in 1674 older (aged >53 years; 17% AD, 39% mild cognitive impairment [MCI]) and 467 young (16–30 years) adults. An AD polygenic risk score combining common risk variants excluding apolipoprotein E (APOE), and a single nucleotide polymorphism in TREM2, were both associated with reduced hippocampal volume in healthy older adults and those with MCI. APOE ɛ4 was associated with hippocampal and amygdala volume in those with AD and MCI but was not associated in healthy older adults. No associations were found in young adults. Genetic risk for AD affects the hippocampus before the clinical symptoms of AD, reflecting a neurodegenerative effect before clinical manifestations in older adults.

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“…Although the hippocampus has traditionally captured more attention than the amygdala, both structures are critically involved in memory processes and present a similar degree of volume loss in AD3435. Nevertheless, it remains to be determined whether amygdala atrophy, like hippocampal atrophy36, accounts for the emotional changes occurring with disease progression.…”

Section: Discussionmentioning

confidence: 99%

Atrophy of amygdala and abnormal memory-related alpha oscillations over posterior cingulate predict conversion to Alzheimer’s disease

Val

Cantero

Atienza

2016

Sci Rep

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Synaptic dysfunction, a key pathophysiological hallmark of Alzheimer’s disease (AD), may account for abnormal memory-related EEG patterns in prodromal AD. Here, we investigate to what extent oscillatory EEG changes during memory encoding and/or retrieval enhance the accuracy of medial temporal lobe (MTL) atrophy in predicting conversion from amnestic mild cognitive impairment (aMCI) to AD. As expected, aMCI individuals that, within a 2-year follow-up period, developed dementia (N = 16) compared to healthy older (HO) (N = 26) and stable aMCI (N = 18) showed poorer associative memory, greater MTL atrophy, and lower capacity to recruit alpha oscillatory cortical networks. Interestingly, encoding-induced abnormal alpha desynchronized activity over the posterior cingulate cortex (PCC) at baseline showed significantly higher accuracy in predicting AD than the magnitude of amygdala atrophy. Nevertheless, the best accuracy was obtained when the two markers were fitted into the model (sensitivity = 78%, specificity = 82%). These results support the idea that synaptic integrity/function in the PCC is affected during prodromal AD and has the potential of improving early detection when combined with MRI biomarkers.

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Amygdalar Atrophy in Early Alzheimer’s Disease

Cited by 50 publications

References 79 publications

Naringenin protects AlCl3/D-galactose induced neurotoxicity in rat model of AD via attenuation of acetylcholinesterase levels and inhibition of oxidative stress

Naringenin protects AlCl3/D-galactose induced neurotoxicity in rat model of AD via attenuation of acetylcholinesterase levels and inhibition of oxidative stress

The effect of increased genetic risk for Alzheimer's disease on hippocampal and amygdala volume

Atrophy of amygdala and abnormal memory-related alpha oscillations over posterior cingulate predict conversion to Alzheimer’s disease

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