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Decrease in acetylcholinergic neurons in the pedunculopontine tegmental nucleus in a patient with Prader‐Willi syndrome
Author(s) -
Hayashi Masaharu,
Miyata Rie,
Tanuma Naoyuki
Publication year - 2011
Publication title -
neuropathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.701
H-Index - 61
eISSN - 1440-1789
pISSN - 0919-6544
DOI - 10.1111/j.1440-1789.2010.01157.x
Subject(s) - hypotonia , nucleus basalis , pedunculopontine tegmental nucleus , pars compacta , pedunculopontine nucleus , endocrinology , neuroscience , medicine , cerebral cortex , nucleus , biology , acetylcholine , cholinergic neuron , deep brain stimulation , dopamine , substantia nigra , parkinson's disease , dopaminergic , disease
Prader‐Willi syndrome (PWS) is caused by the absence of paternally contributed genes in chromosome 15, and is characterized by hypotonia, feeding difficulty, mental retardation, growth failure, hypogonadism and severe obesity. To elucidate the pathogenesis of neurological disorders, we immunohistochemically examined the γ‐aminobutyric acid (GABA)ergic interneurons (GABAis) in the cerebral cortex and acetylcholine neurons (AchNs) in the nucleus basalis of Meynert (MyN) and pedunculopontine tegmental nucleus pars compacta (PPNc) in an autopsy case of one PWS patient with a deletion in the 15q11‐q12 region and three control patients. The GABAis in the cerebral cortex and AchNs in the MyN were well preserved in the PWS patient. The AchNs in the PPNc in the PWS patient were severely reduced in comparison with those in controls, whereas catecholaminergic neurons and GABAis were preserved. The selective loss of AchNs in the PPNc may be involved in hypotonia and/or REM sleep abnormalities in PWS patients.