bioRxivEvolutionary Biology
Evolution of Human-specific Alleles Protecting Cognitive Function of Grandmothers
S. Saha, N. Khan, T. Comi, A. Verhagen, A. Sasmal, S. Diaz, H. Yu, X. Chen, J. M. Akey, M. Frank, P. Gagneux, A. Varki
Abstract
Late-onset Alzheimers Disease (LOAD) pathology is rare in our closest living evolutionary relatives (chimpanzees), which also express much lower microglial levels of CD33(Siglec-3)-a myelomonocytic receptor inhibiting innate immune reactivity by extracellular V-set domain recognition of sialic acid(Sia)-containing "self-associated molecular patterns" (SAMPs). We earlier showed that V-set domain-deficient CD33-variant allele, protective against LOAD, is derived and specific to hominin-lineage. We now report that CD33 also harbors multiple hominin-specific V-set domain mutations and explore selection forces that may have favored such genomic changes. N-glycolylneuraminic acid (Neu5Gc), the preferred Sia-ligand of ancestral CD33 is absent in humans, due to hominin-specific, fixed loss-of-function mutation in CMAH, which generates CMP-Neu5Gc from its precursor, CMP-N-acetylneuraminic acid (Neu5Ac). Extensive mutational analysis and MD-simulations indicate that fixed change in amino acid 21 of hominin V-set domain and conformational changes related to His45 corrected for Neu5Gc-loss by switching to Neu5Ac-recognition. Considering immune-evasive "molecular mimicry" of SAMPs by pathogens, we found that human-specific pathogens Neisseria gonorrhoeae and Group B Streptococcus (affecting fertility and fetuses/neonates respectively) selectively bind huCD33 and this binding is significantly impacted by amino acid 21 modification. Alongside LOAD-protective CD33 alleles, humans harbor additional, derived, population-universal, cognition-protective variants absent in "great ape" genomes. Interestingly, 11 of 13 SNPs in these human genes (including CD33), that protect the cognitive health of elderly populations, are not shared by genomes of archaic hominins: Neanderthals and Denisovans. Finally, we present a plausible evolutionary scenario to compile, correlate and comprehend existing knowledge about huCD33 evolution and suggest that grandmothering emerged in humans.
- organism: human
- assay: DNA methylation
- assay: whole-genome sequencing
- research focus: chromatin & epigenetic regulation
- research focus: gene regulatory network inference
- approach: statistical model
Reproducibility ledger
Nobody has reported trying to reproduce this paper yet. Did you replicate an experiment or run the code? Your report saves the next lab a week.
Sign in to file a reproducibility report.
Related papers
- CD33-CD45 Interaction Reveals a Mechanistic Link to Alzheimer's Disease Susceptibility
Nicole Vo, Cory D. Rillahan, … Elizabeth M. Bradshaw·bioRxiv·Jul 28, 2025
- CD33 and Clusterin Interact Biophysically and Genetically to Modulate Alzheimer Risk
Roger B. Dodd, Masahiro Enomoto, … Peter St George‐Hyslop·DOAJ (DOAJ: Directory of Open Access Journals)Peer-reviewed·Jul 1, 2026
- Alzheimer's disease associated isoforms of human CD33 distinctively modulate microglial cell responses in 5XFAD mice
Ghazaleh Eskandari‐Sedighi, Madeline C. Crichton, … Matthew Scott Macauley·bioRxiv·Jul 4, 2023
- Evidence for reduced somatic T-cell receptor sequence diversity profiles among Midwestern Amish in an aging cohort study
Lauren A. Cruz, Shiying Liu, … Dana C. Crawford·Annals of Human GeneticsPeer-reviewed·Oct 18, 2026
- TACR3 variant confers resilience to aging and Alzheimer's disease
Nicolas Ruffini, Florian Udo Fischer, … the Frontotemporal Lobar Degeneration Neuroimaging Initiative·medRxiv·Jun 8, 2026
- A Chronological Atlas of Natural Selection in the Human Genome during the Past Half-million Years