Here are the findings from this recent paper:
1. The very derived downstream clades of R1b like R1b1a2a1a2c were well-established in Ireland by 3750 before the present. There is no evidence the ancient specimens in the paper were the first generation in Ireland, so it is likely they were present by 2000 BCE.
2. The population of the Central European migrants to Ireland, who were herders, and had some Steppe-derived ancestry, were MUCH higher, compared to hunter gatherers. In other words, R1b is so common in Ireland because of massive migration of such people.
3. This is emphatically NOT consistent with pioneer colonization and elite dominance.
4. The current distributions in many parts of Western Europe are due to a LACK of invasions since (no Anglo-Saxon or Roman penetration.) In other words, this was a second but more prounounced founder effect of sorts.
5. This is consistent with comparisons to more centrally located, easy to reach locales, like Italy, where the genomes show greater variability in both autosomes and Y DNA, due to introgressions that occurred after the late Neolithic and early Bronze Age migrations. (Cavalli-Sforza's admonishment to understand the difference between an expansion and an "impansion" come to mind.)
6. In Western Europe, Bell Beaker culture is the most likely candidate for the spread of R1b and related autosomal genes.
7. R1b and this Western European expansion is strongly scientifically correlated to lactose persistence, which likely provided the demographic advantage to propagate in larger numbers in places like Hibernia.
8. As an addendum, the megaliths of Western Europe are indeed likely linked to early cardial cultures, who bore of mix of HG and farming genes, which correlate to I-M26 in Ireland and Sardinia.