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Immunocytochemistry and in situ hybridization for tyrosine hydroxylase (TH) were used to study the distribution of putative catecholaminergic neurons in the basal forebrain magnocellular complex (BFMC) of monkeys and humans. Magnocellular TH-expressing neurons in the primate BFMC are distributed along a rostrocaudal gradient, with the largest proportion of these cells located in the medial septal
Cholinergic neurons of the basal nucleus complex (BNC) respond to nerve growth factor (NCF), the first member of a polypeptide gene family that also includes brain‐derived neurotrophic factor (BDNF), neurotrophin‐3 (NT‐3), and neurotrophin‐4/5 (NT‐4/5), NGF, BDNF, and NT‐3 are enriched in hippocampus. In addition, NGF and, more recently, BDNF have been shown to stimulate the cholinergic differenti
Alzheimer's disease (AD) neuropathology is characterized by accumulation of "senile" plaques (SPs) and neurofibrillary tangles (NFTs) in vulnerable brain regions. SPs are principally composed of aggregates of up to 42/43 amino acid β-amyloid (Aβ) peptides. The discovery of familial AD (FAD) mutations in the genes for the amyloid precursor protein (APP) and presenilins (PSs), all of which increase
Immunotherapy approaches for Alzheimer disease currently are among the leading therapeutic directions for the disease. Active and passive immunotherapy against the β-amyloid peptides that aggregate and accumulate in the brain of those afflicted by the disease have been shown by numerous groups to reduce plaque pathology and improve behavior in transgenic mouse models of the disease. Several ongoin
In this review, the case is made that amyloid-β peptide in the brain of patients with Alzheimer's disease is a primary cause of the disease and that immunotherapy directed against this peptide has the potential to halt and/or reverse disease progression. This supposition is supported by the capacity of anti-β-amyloid peptide antibodies to prevent or reverse the disease in mouse models of Alzheimer
Over the past decade, the prevailing view for the molecular and cellular pathogenesis of Alzheimer's disease (AD) has centred on the β-amyloid (Aβ) peptide that accumulates in vulnerable brain areas in the disease. The amyloid cascade hypothesis postulates that the build up of Aβ in the brain causes damage to neurons, leading to dysfunction and loss of neurons, and the clinical phenotype of the am
In molecular neurobiology, perhaps no molecule has been as thoroughly examined as Alzheimer's beta-amyloid precursor protein (beta-APP). In the years since the cDNA encoding beta-APP was cloned, the protein has been the subject of unparalleled scrutiny on all levels. From molecular genetics and cellular biology to neuroanatomy and epidemiology, no scientific discipline has been left unexplored - a
Colchicine may induce a myoneuropathy in patients with renal insufficiency. To date, myotonia has not been described in this disorder. We recently studied 4 patients treated with routine doses of colchicine who, in the setting of renal insufficiency, developed a severe myoneuropathy characterized by prominent myotonic discharges on electromyography. In addition, 1 of the 4 patients had profound cl
Objective: To describe two patients with mesencephalic midline clefts and associated eye movement disorders. Design: Case reports. Results: The first patient developed bilateral internuclear ophthalmoplegia with exotropia, reduced convergence, right ptosis, right fourth-nerve palsy, and right elevator palsy several years after meningitis with hydrocephalus. The second patient had bilateral internu
Transgenic mice developing β-amyloid (Aβ) plaques are advancing experimental treatment strategies for Alzheimer's disease. The metal chelator, clioquinol, is reported by Cherny et al. (2001) to reduce Aβ plaques, presumably by chelation of Aβ-associated zinc and copper. This and other recent Aβ-modulating treatment approaches are discussed.
Post-mortem studies of the brain of an Alzheimer patient indicate fewer senile plaques in the crests of cortical gyri underneath an omental transposition than in neighboring cortical areas.
In molecular neurobiology, perhaps no molecule has been as thoroughly examined as Alzheimer's beta-amyloid precursor protein (betaAPP). In the ten years since the cDNA encoding betaAPP was cloned, the protein has been the subject of unparalleled scrutiny on all levels. From molecular genetics and cellular biology to neuroanatomy and epidemiology, no scientific discipline has been left unexplored -
This article presents a study of transmission through arrays of periodic sub-wavelength apertures. Fundamental limitations for this phenomenon are formulated as a sum rule, relating the transmission coefficient over a bandwidth to the static polarizability. The sum rule is rigorously derived for arbitrary periodic apertures in thin screens. By this sum rule we establish a physical bound on the tra
