Which neurotransmitter causes alzheimers

Iqbal, K. Tau pathology in Alzheimer disease and other tauopathies. Acta , — Iwakiri, M. Neuropathology 29, — Jack, C.

Lancet Neurol. Jiang, S. Jo, S. Johnston, G. Australaisian society for clinical and experimental pharmacologists and toxicologists. Jung, J. Kanekiyo, T. Neuron 81, — Kehrer, C. Altered excitatory-inhibitory balance in the NMDA-hypofunction model of schizophrenia. Kleschevnikov, A. Hippocampal long-term potentiation suppressed by increased inhibition in the Ts65Dn mouse, a genetic model of down syndrome.

Knoferle, J. Knust, H. Kolarova, M. Structure and pathology of tau protein in Alzheimer disease. Alzheimers Dis. Lasarge, C. Neuroscience , — Lee, B. Le Freche, H. Tau phosphorylation and sevoflurane anesthesia: an association to postoperative cognitive impairment. Anesthesiology , — Leung, L. Apolipoprotein E4 causes age- and sex-dependent impairments of hilar GABAergic interneurons and learning and memory deficits in mice. PLoS One 7:e Levy-Lahad, E.

Science , — Li, G. GABAergic interneuron dysfunction impairs hippocampal neurogenesis in adult apolipoprotein E4 knockin mice. Cell Stem Cell 5, — Li, Y. Structural biology of presenilin 1 complexes. Limon, A. Liu, D. Lonskaya, I. Regulation of GABA A receptor trafficking, channel activity and functional plasticity of inhibitory synapses. Mahley, R. Apolipoprotein e sets the stage: response to injury triggers neuropathology.

Neuron 76, — Mandelkow, E. Biochemistry and cell biology of tau protein in neurofibrillary degeneration. Cold Spring Harb. Marcade, M. Etazolate, a neuroprotective drug linking GABA A receptor pharmacology to amyloid precursor protein processing. Marshall, F. GABA B receptors function as heterodimers. Marttinen, M. Synaptic dysfunction and septin protein family members in neurodegenerative diseases. Mattson, M. Evidence for excitoprotective and intraneuronal calcium-regulating roles for secreted forms of the beta-amyloid precursor protein.

Neuron 10, — McQuail, J. Molecular aspects of age-related cognitive decline: the role of GABA signaling. Mitew, S. Aging 34, — Mizukami, K. Brain Res. Neumann, U. Nilsen, L. Glutamate metabolism is impaired in transgenic mice with tau hyperphosphorylation. Blood Flow Metab. Ohki, Y. Binding of longer Abeta to transmembrane domain 1 of presenilin 1 impacts on Abeta42 generation.

Palop, J. Neuron 55, — Parodi, J. Pedersen, J. Postina, R. However, these neurotransmitters may have a role in causing oxidative stress, which is known to be involved in AD pathogenesis. Metabotropic and ionotropic neurotransmitter receptors are localized to the postsynaptic membrane.

Metabotropic receptors are membrane receptors that act through a secondary messenger, whereas ionotropic receptors are ligand-gated channels Fig. These are the major therapeutic targets for AD prevention. Ravi Rajmohan and P. Cynthia L. Bethea and colleagues discuss the role of the neurotransmitter serotonin in altering the mood and anxiety levels of persons with overt symptoms of AD [ 13 ]. They review recent literature on AD, depression, and serotonin. They present research that points to a link between increased depression in women and a higher prevalence of AD.

They discuss serotonin neuron viability in AD progression, the involvement of the caspase-independent pathway, and apoptosis-inducing factors in serotonin-neuron viability, as well as gene expression related to neurodegeneration and neuron viability in AD progression, in adult and aged menopausal macaques.

Their article focuses on ovarian steroids, particularly estrogen, which are crucial for the production of serotonin and for neuronal health. Saurabh Kumar Jha and colleagues discuss stress-induced synaptic dysfunction and neurotransmitter release in AD [ 18 ]. They emphasize that communication between neurons at synaptic junctions is an elegant process that facilitates the transmission of various electro-chemical signals in the central nervous system.

They discuss mechanisms associated with the alteration of signal transmission across synapses in the neocortex and hippocampus— alterations that lead to insidious cognitive and memory decline in AD. Rui Wang and P. Excitatory glutamatergic neurotransmission via NMDAR is critical for synaptic plasticity and survival of neurons. Studies indicate that NMDAR-mediated responses are induced by regionalized receptor activities, followed by different downstream signaling pathways.

Ramesh Kandimalla and P. Hemachandra Reddy update research into therapeutics of neurotransmitters in AD pathogenesis and progression [ 20 ]. They assess the latest developments in neurotransmitter research that use cell and mouse models of AD. They also review clinical trials studying the impact of neurotransmitter agonists and antagonists in persons with AD. Lan Guo and colleagues discuss the association between mitochondrial dysfunction and synaptic transmission deficits in AD [ 21 ].

Impaired mitochondrial energy production, deregulated mitochondrial calcium handling, and excess mitochondrial reactive oxygen species ROS generation and release play important roles in mediating the deregulation of synaptic transmission in AD. They also explain mechanisms by which synapses are injured in particular AD-related conditions. They suggest that a better understanding of mitochondrial dysfunction and synaptic stress in AD may lead to therapeutic strategies that target mitochondrial deficits and that protect synaptic transmission known to be affected in AD [ 21 ].

Synaptic damage, an early pathological event in AD, correlates strongly with increased cognitive deficits and memory loss [ 22 ]. Mitochondria are essential organelles that supply the nucleuotide adenosine triphosphate ATP for several synaptic functions.

This mechanism suggests that mitochondria are the promising targets of new therapeutics inAD [ 22 ]. Abstract Alzheimer's disease is characterized by markedly reduced concentration of acetylcholine in hippocampus and neocortex, caused by degeneration of cholinergic neurons. Publication types English Abstract Review. Substances Neurotransmitter Agents. Wu, Z. Guo, M. Gearing, and G. Tackenberg, S. Grinschgl, A. Trutzel, et al. Masson, M. Emerit, M. Hamon, and M. Glikmann-Johnston, M. Saling, D.

Reutens, and J. Monaco, K. Gebhardt, S. Chlebowski, et al. Neurotrauma , 31 , No. Welford, M. Vercauteren, A. Tajeddinn, T. Persson, S. Maioli, et al. Persson, J.

Calvo-Garrido, et al. Alzheimers Dis. Zhang and R. Zhang, H. Cohen, et al. Marner, G. Knudsen, K. Madsen, et al. Pitychoutis, A. Belmer, I. Moutkine, et al. Gibbs and L. Hagena and D. Pascual-Brazo, E. Yun and H. In Vitro , 25 , No. Stiedl, E. Konradsson-Geuken, and S. Zareifopoulos and C. Chamberlain and T. Aston-Jones and B.

Vetreno, R. Ramos, S. Anzalone, and L. Rajabi, A. Shamsizadeh, H. Amini, et al. Toneff, L. Funkelstein, C. Mosier, et al. Chen, Y. Peng, P. Che, et al. Thathiah, K. Snellinx, et al.

Uematsu, B.