Nucleus of Meynert

Irle E, Markowitsch HJ (1986) Afferent connections of the substantia innominata/basal nucleus of Meynert in carnivores and primates. J Hirnforsch 27 343-367. 

The other important source of free radicals comes from redox-active metals. Strikingly, NFT and A() plaques were found coincident with overaccumulation of iron in the hippocampus, cerebral cortex, and basal nucleus of Meynert (Lovell et al.,... 

Subcortical nuclei basal nucleus of Meynert, amygdala, and substantia nigra... 

Neurochemical examination of biopsy and antopsy brain material from Alzheimer patients has revealed loss of the presynaptic marker enzymes acetyl coenzyme A (acetyl-CoA), chohne 6>-acetyltransferase and acetylcholinesterase (AChE), and of muscarinic receptor sites of the M2 subtype correlating with dementia score and severity of nenrohistopathology [8]. These alterations do, to some extent, reflect the well-documented neuronal cell loss in the nucleus of Meynert in presenile dementia and AD. Lesions of this brain nncleus in rats, a limited model for the cholinergic deficit of AD, resnlt in marked reductions in the levels of cholinergic en me markers in the neocortex accompanied by great decreases in the total muscarinic receptor levels [9,10]. 

Manfridi, A., Brambilla, D. Mancia, M. (1999). Stimulation of NMDA and AMPA receptors in the rat nucleus basalis of Meynert affects sleep. Am. J. Physiol. 277, R1488-92. 

The neural structures involved in the promotion of the waking (W) state are located in the (1) brainstem [dorsal raphe nucleus (DRN), median raphe nucleus (MRN), locus coeruleus (LC), laterodorsal and pedunculopontine tegmental nuclei (LDT/PPT), and medial-pontine reticular formation (mPRF)] (2) hypothalamus [tuberomammillary nucleus (TMN) and lateral hypothalamus (LH)[ (3) basal forebrain (BFB) (medial septal area, nucleus basalis of Meynert) and (4) midbrain ventral tegmental area (VTA) and substantia nigra pars compacta (SNc) (Pace-Schott Hobson, 2002 Jones, 2003). The following neurotransmitters function to promote W (1) acetylcholine (ACh LDT/PPT, BFB) (2) noradrenaline (NA LC) (3) serotonin (5-HT DRN, MRN) (4) histamine (HA TMN) (5) glutamate (GLU mPRF, BFB, thalamus) (6) orexin (OX LH) and (7) dopamine (DA VTA, SNc) (Zoltoski et al, 1999 Monti, 2004). 

Nucleus basalis of Meynert One of the forebrain structures where neurodegeneration occurs in Alzheimer s disease. 

Dubelaar, E.J., Verwer, R.W., Hofman, M.A., Van Heerikhuize, J.J., Ravid, R., Swaab, D.E. (2004) APOE epsilon4 genotype is accompanied by lower metaboUc activity in nucleus basalis of Meynert neurons in Alzheimer patients and controls as indicated by the size of the Golgi apparatus. J. Neuropathol. Exp. Neurol, 63, 159-169. 

The cholinergic pathways in the mammalian brain are extremely diffuse and arise from cell bodies located in the hindbrain and the midbrain. Of these areas, there has been considerable interest of late in the nucleus basalis magnocellularis of Meynert because this region appears to be particularly affected in some patients with familial Alzheimer s disease. As the projections from this area innervate the cortex, it has been speculated... 

Figure 1. Frontal section through human brain stained for acetylcholinesterase (frame A) and diagram showing locations of individual cholinergic cells irregularly dispersed throughout the nucleus basalis of Meynert and surrounding regions of human brain (frame B). Abbreviations AC, anterior commissure B, nucleus basalis of Meynert gpe, globus pallidus external part gpi, globus pallidus internal part, 1C internal capsule P, putamen.

The rapid, low amplitude EEG activity of REM sleep, like that of waking, is sustained by cholinergic processes (Kinai Szerb, 1965 Phillis 8c Ghong, 1965), principally from neurons in the basal forebrain which project over the entire cortex (Divac, 1975 Lehmann et al., 1980 Bigl et al., 1982). Activation of the nucleus basalis of Meynert results in acetylcholine release in the cortex... 

Cholinesterase inhibitors cross the blood-brain barrier and decrease enzymatic hydrolysis of acetylcholine in the synaptic cleft, thereby increasing acetylcholine availability for neurotransmission. The rationale for using cholinergic agents to treat Alzheimer s disease stems from evidence of decreased cerebral choline acetyltrans-ferase (the enzyme responsible for acetylcholine synthesis) and cholinergic neuron loss in the nucleus basalis of Meynert, which correlate with plaque formation and cognitive impairment (Arendt et al. 1985 Davies and Maloney 1976 Etienne et al. 1986 Perry et al. 1978b). 

Amyloid cascade hypothesis of Alzheimer s disease. A leading contemporary theory for the biological basis of Alzheimer s disease centers around the formation of beta amyloid. Certainly much of this amyloid destroys cholinergic neurons in the nucleus basalis of Meynert (Fig. 12—11), although the damage becomes more widespread as the disease progresses (Fig. 12-13). Hypothetically, Alzheimer s disease is a disorder in which beta amyloid deposition destroys neurons, in a manner somewhat analogous to that in which the abnormal deposition of cholesterol causes atherosclerosis. Thus,... 

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