Altered cortical plasticity but preserved cholinergic transmission in HIV-associated dementia: A TMS study

We used transcranial magnetic stimulation (TMS) to examine whether short-latency afferent inhibition (SAI)-a marker of cholinergic transmission-and long-term potentiation (LTP)-like cortical plasticity via paired associative stimulation (PAS25) are affected in patients with HIV-associated dementia (HAD).

Seventeen HAD and 17 age-matched healthy controls (HCs) underwent SAI assessment; 15 subjects per group also completed PAS25. Resting motor threshold (RMT) and motor evoked potentials (MEPs) were recorded. SAI was measured as the ratio of conditioned to unconditioned MEPs, using peripheral stimulation followed by motor cortex TMS. PAS25 consisted of 180 paired peripheral-cortical stimuli at 0.2 Hz; MEPs were recorded at baseline, 0, 15, and 30 min (T0, T15, T30) post-intervention.

RMT and SAI did not differ between HAD and HCs (RMT: 54.0 ± 7.8 vs. 50.7 ± 6.1; SAI: 46.9 ± 8.6 % vs. 44.9 ± 5.3 %). PAS25 significantly increased MEPs amplitude in HCs at all timepoints (RTEs: T0 = 0.76, T15 = 0.87, T30 = 0.80), but not in HAD (T0 = 0.31, T15 = 0.29, T30 = 0.26).

In HAD, cholinergic activity is preserved in motor cortex, while glutamate-dependent LTP-like plasticity is impaired.

SAI and PAS25 are complementary neurophysiological tools distinguishing HAD from Alzheimer's disease.