Astrocytic and microglial nicotinic acetylcholine receptors: an overlooked issue in Alzheimer’s disease

Abstract

It is increasingly recognized that astrocytes and microglia-associated dysfunction contribute to AD pathology. In addition, glial nicotinic acetylcholine receptors (nAChRs) play a role in AD-related phenomena, such as neuron survival, synaptic plasticity, and memory. From mechanistic point of view, the glial regulation of pro-inflammatory cytokines, as common contributors in AD, is modulated by nAChRs. Astrocytic and microglial nAChRs contribute to Aβ metabolism, including Aβ phagocytosis and degradation as well as Aβ-related oxidative stress and neurotoxicity. These receptors are also involved in neurotransmission and gliotransmission through indirect interaction with N-Methyl-D-aspartate (NMDA) and a-amino-3-hydroxy-5-methyl-4 isoxazolepropionic acid (AMPA) receptors as well as gamma-aminobutyric acid (GABA) and intracellular calcium regulation. In addition, glial nAChRs participate in trophic factors-induced neuroprotection. This review gathers the most recent advances along with the previous data on astrocytic and microglial nAChRs role in AD pathogenesis.

Asn194Lys mutation in RVG29 peptide increases GFP transgene delivery by endocytosis to neuroblastoma and astrocyte cells

“…Moreover, it is possible that the trophism of RVG is not only linked to neurons but also to glial cells. Glial nAChRs participate in trophic factor‐induced neuroprotection . However, glial cells are responsible for the progression of Parkinson's disease and play an important role in initiating the early tissue response.…”

Possible neuromodulating role of different grape (Vitis vinifera L.) derived polyphenols against Alzheimer’s dementia: treatment and mechanisms

“…The cumulative effects of both oxidative stress and neuroinflammation contribute to AD neuropathogenesis; it seems that oxidative stress precedes the deposition of Aβplaques (Wahlster et al 2013). Moreover, microglial and astrocytic activation contributes to the neurodegeneration and enhances Aβ-neurotoxicity (Sadigh-Eteghad et al 2016).…”

Residues Responsible for the Selectivity of α-Conotoxins for Ac-AChBP or nAChRs

“…Consequentially, nAChRs are drug targets for the treatment of severe pain, cognitive decline, epilepsy, and nicotine addiction [1,2,3,4,5]. α-Conotoxins, which come from sea Conus snails, are important tool for studying nAChRs.…”