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A Map of Transcriptomic Signatures of Different Brain Areas in Alzheimer’s Disease

Ferrari, Riccardo Rocco, Fantini, Valentina, Garofalo, Maria, Di Gerlando, Rosalinda, Dragoni, Francesca, Rizzo, Bartolo, Spina, Erica, Rossi, Michele, Calatozzolo, Chiara, Profka, Xhulja, Ceroni, Mauro, Guaita, Antonio, Davin, Annalisa, Gagliardi, Stella, Poloni, Tino Emanuele·2024·International Journal of Molecular Sciences
DOI 10.3390/ijms252011117PMC PMC11508373
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Abstract

Alzheimer’s disease (AD) is a neurodegenerative disorder that progressively involves brain regions with an often-predictable pattern. Damage to the brain appears to spread and worsen with time, but the molecular mechanisms underlying the region-specific distribution of AD pathology at different stages of the disease are still under-investigated. In this study, a whole-transcriptome analysis was carried out on brain samples from the hippocampus (HI), temporal and parietal cortices (TC and PC, respectively), cingulate cortex (CG), and substantia nigra (SN) of six subjects with a definite AD diagnosis and three healthy age-matched controls in duplicate. The transcriptomic results showed a greater number of differentially expressed genes (DEGs) in the TC (1571) and CG (1210) and a smaller number of DEGs in the HI (206), PC (109), and SN (60). Furthermore, the GSEA showed a difference between the group of brain areas affected early (HI and TC) and the group of areas that were subsequently involved (PC, CG, and SN). Notably, in the HI and TC, there was a significant downregulation of shared DEGs primarily involved in synaptic transmission, while in the PC, CG, and SN, there was a significant downregulation of genes primarily involved in protein folding and trafficking. The course of AD could follow a definite time- and severity-related pattern that arises from protein misfolding, as observed in the PC, CG, and SN, and leads to synaptic impairment, as observed in the HI and TC. Therefore, a map of the molecular and biological processes involved in AD pathogenesis may be traced. This could aid in the discovery of novel biological targets in order to develop effective and well-timed therapeutic approaches.

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  • Previous transcriptomic studies and investigations into cortical synaptic density in AD have underscored the link between synaptic transmission and AD pathogenesis, demonstrating that disruptions in synaptic integrity contribute to cortical thinning in AD.

    “Other previous transcriptomic studies and investigations into cortical synaptic density in AD have underscored the link between synaptic transmission and AD pathogenesis, demonstrating that disruptions in synaptic integrity contribute to cortical thinning in AD [74, 75].”

    From Association of APOC1 with cortical atrophy during conversion to Alzheimer’s disease (2025) · cites this paper as [74]

  • Our findings reinforce the connection between synaptic dysfunction and AD pathogenesis, suggesting that disruptions in synaptic integrity contribute to cortical thinning and cognitive decline.

    “Our findings, consistent with previous studies [72, 74–76], reinforce the connection between synaptic dysfunction and AD pathogenesis, suggesting that disruptions in synaptic integrity contribute to cortical thinning and cognitive decline.”

    From Association of APOC1 with cortical atrophy during conversion to Alzheimer’s disease (2025) · cites this paper as [74]

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Authors
Ferrari, R. R., Fantini, V., Garofalo, M., Di Gerlando, R., Dragoni, F., Rizzo, B., Spina, E., Rossi, M., Calatozzolo, C., Profka, X., Ceroni, M., Guaita, A., Davin, A., Gagliardi, S., & Poloni, T. E.
Affiliations
  • Department of Brain and Behavioral Sciences, University of Pavia, Viale Golgi 19, 27100 Pavia, Italy
  • Laboratory of Neurobiology and Neurogenetics, Golgi Cenci Foundation, Corso San Martino 10, 20081 Abbiategrasso, Italy
  • Molecular Biology and Transcriptomic Unit, IRCCS Mondino Foundation, Via Mondino 2, 27100 Pavia, Italy
  • Unity of Biostatistics, Golgi Cenci Foundation, Corso San Martino 10, 20081 Abbiategrasso, Italy
  • Department of Neurology and Neuropathology, Golgi Cenci Foundation, Corso San Martino 10, 20081 Abbiategrasso, Italy
ORCID
Venue
International Journal of Molecular Sciences
Publisher
MDPI AG
Published
2024-10-16
Volume
25
Issue
20
Pages
11117
ISSN
1422-0067
DOI
10.3390/ijms252011117
PMC
PMC11508373
Cited by
14
References
13
Language
en
Licence
creativecommons.org/licenses/by/4.0/ (vor)
Funders
  • Serpero Foundation (20129, 20081)
  • Golgi Cenci Foundation (20129, 20081)

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