scholarly journals Foveal Avascular Zone and Choroidal Thickness Are Decreased in Subjects with Hard Drusen and without High Genetic Risk of Developing Alzheimer’s Disease

Biomedicines ◽  
2021 ◽  
Vol 9 (6) ◽  
pp. 638
Author(s):  
Inés López-Cuenca ◽  
Rosa de Hoz ◽  
Celia Alcantara-Rey ◽  
Elena Salobrar-García ◽  
Lorena Elvira-Hurtado ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Genetic Risk ◽  
Choroidal Thickness ◽  
Apoe Gene ◽  
Age Related Macular Degeneration ◽  
Foveal Avascular Zone ◽  
Vascular Changes ◽  
Avascular Zone ◽  
E4 Allele

A family history (FH+) of Alzheimer’s disease (AD) and ɛ4 allele of the ApoE gene are the main genetic risk factors for developing AD, whereas ɛ4 allele plays a protective role in age-related macular degeneration. Ocular vascular changes have been reported in both pathologies. We analyzed the choroidal thickness using optical coherence tomography (OCT) and the foveal avascular zone (FAZ) using OCT-angiography and compared the results with ApoE gene expression, AD FH+, and the presence or absence of hard drusen (HD) in 184 cognitively healthy subjects. Choroidal thickness was statistically significantly different in the (FH−, ɛ4−, HD+) group compared with (i) both the (FH−, ɛ4−, HD−) and the (FH+, ɛ4+, HD+) groups in the superior and inferior points at 1500 μm, and (ii) the (FH+, ɛ4−, HD+) group in the superior point at 1500 μm. There were statistically significant differences in the superficial FAZ between the (FH+, ɛ4−, HD+) group and (i) the (FH+, ɛ4−, HD−) group and (ii) the (FH+, ɛ4+, HD−) group. In conclusion, ocular vascular changes are not yet evident in participants with a genetic risk of developing AD.

scholarly journals Ocular vascular changes in relatives at high genetic risk for developing Alzheimer’s disease: foveal avascular zone and choroidal thickness

2022 ◽  
Vol 100 (S267) ◽  
Author(s):  
Inés López‐Cuenca ◽  
Elena Salobrar‐Garcia ◽  
Celia Alcántara‐Rey ◽  
Lorena Elvira‐Hurtado ◽  
José A. Fernández‐Albarral ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Genetic Risk ◽  
Choroidal Thickness ◽  
Foveal Avascular Zone ◽  
Vascular Changes ◽  
High Genetic Risk ◽  
Avascular Zone

scholarly journals Ocular Vascular Changes in Mild Alzheimer’s Disease Patients: Foveal Avascular Zone, Choroidal Thickness, and ONH Hemoglobin Analysis

2020 ◽  
Vol 10 (4) ◽  
pp. 231
Author(s):  
Elena Salobrar-Garcia ◽  
Carmen Méndez-Hernández ◽  
Rosa de Hoz ◽  
Ana I. Ramírez ◽  
Inés López-Cuenca ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Choroidal Thickness ◽  
Foveal Avascular Zone ◽  
Vascular Density ◽  
Vascular Changes ◽  
Smooth Musculature ◽  
Avascular Zone ◽  
Early Biomarker ◽  
The Brain

In Alzheimer’s disease (AD), vascular changes could be caused by amyloid beta (Aβ) aggregates replacing the contractile smooth musculature of the arteriole walls. These changes happen in the brain vascular network, but also in the eye, and are related to decreased vascular density and low blood flow. In patients with Alzheimer’s disease, thinning of the choroid and the retina has been shown. The aim of this prospective study was to assess the retinal and choroidal vascular systems, analyzing the choroidal thickness with optical coherence tomography (OCT), the foveal avascular zone (FAZ) with OCT-angiography (OCTA), and the optic nerve head (ONH) hemoglobin with the Laguna ONhE program, to evaluate which of the two ocular vascular systems shows earlier changes in mild AD patients. These patients, compared to controls, showed a significantly thinner choroid at all the analyzed points, with the exception of the temporal macula (at 1000 and 1500 µm from the fovea). On the other hand, the FAZ and ONH hemoglobin did not show significant differences. In conclusion, a thinner choroid was the main ocular vascular change observed in mild AD patients, while the retinal vessels were not yet affected. Therefore, choroidal thickness could be used an early biomarker in AD.

scholarly journals Ocular Vascular Changes: Choroidal Thickness as an Early Biomarker for Alzheimer’s Disease?

2021 ◽  
Vol 11 (12) ◽  
pp. 1365
Author(s):  
Chiara Villa
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Choroidal Thickness ◽  
The Elderly ◽  
Vascular Changes ◽  
Age Related ◽  
Early Biomarker ◽  
Progressive Disorder

Alzheimer’s disease (AD) is an age-related neurodegenerative and progressive disorder representing the most common form of dementia among the elderly [...]

P3-274: Major genetic risk factors for age-related macular degeneration are not associated with Alzheimer's disease

2008 ◽  
Vol 4 ◽  
pp. T602-T602
Author(s):  
M. Axel Wollmer ◽  
Aleksandra Maruszak ◽  
Magdalini Tsolaki ◽  
Elisabeth Kapaki ◽  
Dietmar R. Thal ◽  
...  
Keyword(s):  
Risk Factors ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Macular Degeneration ◽  
Genetic Risk ◽  
Genetic Risk Factors ◽  
Age Related Macular Degeneration ◽  
Age Related

scholarly journals Changes in retinal microvasculature and retinal layer thickness in association with apolipoprotein E genotype in Alzheimer’s disease

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Joo Youn Shin ◽  
Eun Young Choi ◽  
Min Kim ◽  
Hyung Keun Lee ◽  
Suk Ho Byeon
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Layer Thickness ◽  
Structural Changes ◽  
Foveal Avascular Zone ◽  
Retinal Layer ◽  
Inner Plexiform Layer ◽  
Apoe Ε4 ◽  
Retinal Microvasculature ◽  
Capillary Plexus

AbstractBiomarker tests of Alzheimer’s disease (AD) are invasive and expensive. Recent developments in optical coherence tomography (OCT) and OCT angiography (OCTA) have enabled noninvasive, cost-effective characterization of retinal layer vasculature and thickness. Using OCTA and OCT, we characterized retinal microvascular changes in the mild cognitive impairment (MCI) stage of AD and assessed their correlation with structural changes in each retinal neuronal layer. We also evaluated the effect of the APOE-ε4 genotype on retinal microvasculature and layer thickness. Retinal layer thickness did not differ between MCI patients (40 eyes) and controls (37 eyes, all p > 0.05). MCI patients had lower vessel density (VD) (p = 0.003) of the superficial capillary plexus (SCP) and larger foveal avascular zone area (p = 0.01) of the deep capillary plexus (DCP) than those of controls. VD of the SCP correlated with the ganglion cell layer (r = 0.358, p = 0.03) and inner plexiform layer thickness (r = 0.437, p = 0.007) in MCI patients. APOE-ε4-carrying MCI patients had a lower VD of the DCP than non-carriers (p = 0.03). In conclusion, retinal microvasculature was reduced in patients with AD-associated MCI, but retinal thickness was not changed; these changes might be affected by the APOE genotype. OCTA of the retinal microvasculature may be useful to detect vascular changes in AD.

scholarly journals Interaction of Alzheimer’s Disease-Associated Genetic Risk with Indicators of Socioeconomic Position on Mild Cognitive Impairment in the Heinz Nixdorf Recall Study

2021 ◽  
pp. 1-11
Author(s):  
Mirjam Frank ◽  
Jonas Hensel ◽  
Lisa Baak ◽  
Sara Schramm ◽  
Nico Dragano ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Socioeconomic Position ◽  
Genetic Risk ◽  
Late Onset ◽  
Heinz Nixdorf Recall Study ◽  
Low Education ◽  
Additive Scale

Background: The apolipoprotein E (APOE) ɛ4 allele is reported to be a strong genetic risk factor for mild cognitive impairment (MCI) and Alzheimer’s disease (AD). Additional genetic loci have been detected that influence the risk for late-onset AD. As socioeconomic position (SEP) is also strongly related to cognitive decline, SEP has been suggested to be a possible modifier of the genetic effect on MCI. Objective: To investigate whether APOE ɛ4 and a genetic sum score of AD-associated risk alleles (GRSAD) interact with SEP indicators to affect MCI in a population-based cohort. Methods: Using data of 3,834 participants of the Heinz Nixdorf Recall Study, APOE ɛ4 and GRSAD by SEP interactions were assessed using logistic regression models, as well as SEP-stratified genetic association analysis. Interaction on additive scale was calculated using the relative excess risk due to interaction (RERI). All analysis were additionally stratified by sex. Results: Indication for interaction on the additive scale was found between APOE ɛ4 and low education on MCI (RERI: 0.52 [95% -confidence interval (CI): 0.01; 1.03]). The strongest genetic effects of the APOE ɛ4 genotype on MCI were observed in groups of low education (Odds ratio (OR): 1.46 [95% -CI: 0.79; 2.63] for≤10 years of education versus OR: 1.00 [95% -CI: 0.43; 2.14] for≥18 years of education). Sex stratified results showed stronger effects in women. No indication for interaction between the GRSAD and SEP indicators on MCI was observed. Conclusion: Results indicate that low education may have an impact on APOE ɛ4 expression on MCI, especially among women.

scholarly journals Phospholipid dysregulation contributes to ApoE4-associated cognitive deficits in Alzheimer’s disease pathogenesis

2015 ◽  
Vol 112 (38) ◽  
pp. 11965-11970 ◽  
Author(s):  
Li Zhu ◽  
Minghao Zhong ◽  
Gregory A. Elder ◽  
Mary Sano ◽  
David M. Holtzman ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Deficits ◽  
Genetic Risk ◽  
Primary Neurons ◽  
Loss Of Function ◽  
Sporadic Alzheimer’S Disease ◽  
Postmortem Human Brain ◽  
Apoe4 Allele ◽  
Synaptojanin 1

The apolipoprotein E4 (ApoE4) allele is the strongest genetic risk factor for developing sporadic Alzheimer’s disease (AD). However, the mechanisms underlying the pathogenic nature of ApoE4 are not well understood. In this study, we have found that ApoE proteins are critical determinants of brain phospholipid homeostasis and that the ApoE4 isoform is dysfunctional in this process. We have found that the levels of phosphoinositol biphosphate (PIP2) are reduced in postmortem human brain tissues of ApoE4 carriers, in the brains of ApoE4 knock-in (KI) mice, and in primary neurons expressing ApoE4 alleles compared with those levels in ApoE3 counterparts. These changes are secondary to increased expression of a PIP2-degrading enzyme, the phosphoinositol phosphatase synaptojanin 1 (synj1), in ApoE4 carriers. Genetic reduction of synj1 in ApoE4 KI mouse models restores PIP2 levels and, more important, rescues AD-related cognitive deficits in these mice. Further studies indicate that ApoE4 behaves similar to ApoE null conditions, which fails to degrade synj1 mRNA efficiently, unlike ApoE3 does. These data suggest a loss of function of ApoE4 genotype. Together, our data uncover a previously unidentified mechanism that links ApoE4-induced phospholipid changes to the pathogenic nature of ApoE4 in AD.

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