ABCA7
- Known as:
- ABCA7
- Catalog number:
- 000889A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ABCA7
Related genes to: ABCA7
- Gene:
- ABCA7 NIH gene
- Name:
- ATP binding cassette subfamily A member 7
- Previous symbol:
- -
- Synonyms:
- ABCX
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-06-11
- Date modifiied:
- 2019-03-21
Related products to: ABCA7
Related articles to: ABCA7
- Compromised vascular health is increasingly linked to Alzheimer's disease (AD) risk. Estimated pulse wave velocity (ePWV), derived from age and blood pressure, and provides a practical, non-invasive index of vascular stiffness and overall vascular health. Older African Americans experience a disproportionate burden of vascular disease and AD. Genetic risk factors such as APOE ε4 and ABCA7-80 (rs115550680) further increase AD susceptibility. However, whether these genetic risks influence vascular stiffness and how that may interact with AD pathology remains unknown, especially in African Americans. - Source: PubMed
Publication date: 2026/08/11
Budak MirayHeffernan Kevin SIshaq MartinaParuzel VictoriaAbdalla DemianaMoallemian SoodehFausto Bernadette AElahi Fanny MGluck Mark A - Alzheimer's disease (AD) and type 2 diabetes mellitus (T2DM) share overlapping pathological mechanisms characterized by neuroinflammation and metabolic dysfunction, yet the underlying mechanisms remain elusive. In this study, we aimed to investigate the potential involvement of Abca7 in the microglial responses linking AD and T2DM. Single-cell RNA sequencing (scRNA-seq) data from the hippocampi of db/db and db/m mice were analyzed to characterize cellular heterogeneity. To validate the bioinformatic findings, an AD mouse model was established by a single intracerebroventricular injection of Aβ1-42. Behavioral performances were observed, and the protein expression of Abca7 and typical neuropathological features of AD were detected. In parallel, in vitro studies were conducted using BV2 microglial cells exposed to Aβ1-42 following Abca7 knockdown. The scRNA-seq analysis revealed significant alterations in endothelial cells, microglia, and oligodendrocytes in db/db mice. Microglia emerged as central regulators of neuroinflammatory responses, with Abca7 identified as a hub gene linked to both T2DM and AD pathology. Consistently, the expression of Abca7 in the hippocampus of AD mice was markedly elevated and positively correlated with the cognitive impairments and Aβ/Tau pathology. Moreover, the knockdown of Abca7 could protect BV2 cells against Aβ-induced injuries and hyperactivation which could be partly ascribed to the suppression of NF-κB signaling and oxidative stress. Overall, these results suggest Abca7 may play a linking role in the microglial response between T2DM and AD, which is partly supported by in vivo and in vitro results of its effect on the hyperactivation of microglia in AD-like pathologies. - Source: PubMed
Publication date: 2026/07/16
Cheng MingZheng XinWei Ya-DongGe Jin-Fang - Alzheimer's disease (AD), Parkinson's disease (PD) and Lewy body dementia (LBD) overlap clinically, pathologically and genetically, complicating interpretation of cross-disorder genome-wide association study (GWAS) signals. - Source: PubMed
Publication date: 2026/07/02
Zhang YingZhang ZhishuaiQiu ShizhengHu Yang - Frontotemporal lobar degeneration (FTLD), a major cause of early-onset dementia, includes a heterogeneous group of neurodegenerative disorders with a strong genetic component. Mutations in , , and are found in about 40% of patients with the behavioral variant (bvFTD). More recently, rarer pathogenic variants have been identified in other genes, such as , initially linked to Alzheimer's disease but increasingly implicated in other neurodegenerative conditions. Here we describe a specific variant which has not previously been reported in the literature. - Source: PubMed
Publication date: 2026/05/18
Geron ChloéMaquet Pierre - Alzheimer's disease (AD) shows substantial clinical heterogeneity often caused by genetic variants contributing to both familial and early-onset forms. However, the genetic landscape of AD in the diverse Indian population remains further characterised. To identify probable pathogenic variants associated with AD, representing individuals from Eastern India and to assess their potential structural effects using molecular dynamics (MD) simulations. Whole-exome sequencing was performed in 29 radiologically confirmed AD patients. Variants identified were screened using standard in silico prediction tools and categorised according to their involvement in amyloid precursor protein (APP)-related and non-APP pathways. Molecular dynamics simulations of filtered variants in PSEN1, SORL1, and ABCA7 genes were conducted using GROMACS 2024 to assess conformational stability, flexibility (RMSD, RMSF), compactness (Rg), and solvent accessibility (SASA). Thirty-six variants across 18 genes were identified, including five pathogenic variants and 31 variants of uncertain significance. Frequently affected genes included ABCA7 (8 variants), SORL1 (3 variants), PSEN1 (two novel variants), and APP (London mutation, Val717Ile). Most patients (83.3%) had a positive family history, with a mean age at onset of 54.17 ± 11.74 years, presenting with typical AD, posterior cortical atrophy, or frontal variants. MD simulations revealed increased rigidity, altered electrostatic interactions, and disrupted ATP-binding dynamics in mutant proteins compared with wild type. This study identifies novel and known AD-associated variants in an Indian cohort and demonstrates their potential structural impact. Integrating genetic and structural analyses provides valuable insights into AD pathogenesis in underrepresented populations. - Source: PubMed
Publication date: 2026/07/07
Sadhukhan DipanwitaMukherjee AdreeshKamal Izaz MonirMaitra ShreyosiVedeshachaitanya Brahmachari SomnathBhattacharyya BidishaBiswas AtanuChakrabarti SaikatBiswas Arindam