Alzheimer's disease: Neurofibrillary tangles in nuclei that project to the cerebral cortex

German, Dwight C.; White, Charles L.; Sparkman, Dennis R.

doi:10.1016/0306-4522(87)90123-0

Cited by 199 publications

(77 citation statements)

References 33 publications

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“…A severe neuronal degeneration was observed in the basal nucleus of Meynert, locus coeruleus, the median raphe nucleus, medial amygdaloid nucleus, pedunculopontine tegmental nucleus, and substantia nigra, thereby confirming a number of earlier studies (Herzog and Kemper, 1980;Arendt et al, 1983;Mann et al, 1983;Shortridge et al, 1985;Yamamoto and Hirano, 1985;German et al, 1987;Jellinger, 1988;Woolf et al, 1989;Esiri et al, 1990;Goto et al, 1990;Aletrino et al, 1992;Förstl et al, 1992;Halliday et al, 1992;Scott et al, 1992). The overall extent of degeneration and the gradual variation of cell loss between different areas are also in agreement with previous reports (Zweig et al, 1988;ChanPalay et al, 1992;Arendt et al, 1995c).…”

Section: Apoe Gene Dose and Degeneration Of Subcortical Neuronssupporting

confidence: 78%

Plastic Neuronal Remodeling Is Impaired in Patients with Alzheimer’s Disease Carrying Apolipoprotein ε4 Allele

Arendt¹,

Schindler²,

Brückner³

et al. 1997

J. Neurosci.

309

174

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A relationship between the apolipoprotein E (apoE) genotype and the risk to develop Alzheimer's disease has been established recently. Apolipoprotein synthesis is implicated in developmental processes and in neuronal repair of the adult nervous system.In the present study, we investigated the influence of the apolipoprotein polymorphism on the severity of neuronal degeneration and the extent of plastic dendritic remodeling in Alzheimer's disease. Changes in length and arborization of dendrites of Golgi-impregnated neurons in the basal nucleus of Meynert, locus coeruleus, raphe magnus nucleus, medial amygdaloid nucleus, pedunculopontine tegmental nucleus, and substantia nigra were analyzed after three-dimensional reconstruction. Patients with either one or two apoE ⑀4 alleles not only showed a more severe degeneration in all areas investigated than in patients lacking the apoE 4 allele but also revealed significantly less plastic dendritic changes. ApoE ⑀4 allele copy number, furthermore, had a significant effect on the pattern of dendritic arborization. Moreover, the relationship between the intensity of dendritic growth and both the extent of neuronal degeneration and the stage of the disease seen in patients lacking the apoE ⑀4 allele was very weak in the presence of one ⑀4 allele and completely lost in patients homozygous for the ⑀4 allele.The results provide direct evidence that neuronal reorganization is affected severely in patients with Alzheimer's disease carrying the apoE ⑀4 allele. This impairment of neuronal repair might lead to a more rapid functional decompensation, thereby contributing to an earlier onset and more rapid progression of the disease.

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Section: Apoe Gene Dose and Degeneration Of Subcortical Neuronssupporting

confidence: 78%

Plastic Neuronal Remodeling Is Impaired in Patients with Alzheimer’s Disease Carrying Apolipoprotein ε4 Allele

Arendt¹,

Schindler²,

Brückner³

et al. 1997

J. Neurosci.

309

174

View full text Add to dashboard Cite

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“…Cholinergic degeneration is considered to be an important factor underlying memory deficits in neurological disease, such as dementia of Alzheimer's type, and even some Parkinson patients (10,72,74,79). Severity of dementia, number of plaques and, to some degree, loss of synapses, correlate with the degeneration of the cholinergic system in many Alzheimer's patients (27,65). The precise relationship of the septohippocampal cholinergic system to memory function and symptoms caused by cholinergic neuronal degeneration can be investigated if the model has selective neuronal and terminal loss.…”

Section: The Cholinergic System and Cognitionmentioning

confidence: 99%

Selective Antibody-Induced Cholinergic Cell and Synapse Loss Produce Sustained Hippocampal and Cortical Hypometabolism with Correlated Cognitive Deficits

Browne

Mattsson

et al. 2001

Experimental Neurology

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“…This proposed mechanism is consistent with a report of neuritic plaques and NFTs in the cortex and hippocampus appearing at a younger age than the pathological changes in the dorsal raphe nucleus in Down's syndrome patients, who are predisposed to the early development of AD (Mann et al 1984). Although the 5-HT system lacks a clear topographical relationship between brain stem nuclei and cortical projections, the spatial pattern of cell loss in other neurotransmitter systems such as the noradrenergic system, further suggests a primary process of cortical degeneration in AD (Burke et al 1988;German et al 1987;Marcyniuk et al 1986). …”

Section: Serotonergic Dysfunction In Alzheimer's Diseasementioning

confidence: 99%

Serotonin in Aging, Late-Life Depression, and Alzheimer's Disease: The Emerging Role of Functional Imaging

Meltzer

Smith

DeKosky

et al. 1998

Neuropsychopharmacology

464

240

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(5-HT) neuron and neurotransmitter loss in normal aging and neuropsychiatric diseases of late life may contribute to behavioral changes commonly observed in the elderly population. Extensive evidence implicates a deficit in serotonergic neurotransmission in the development of major depression. It has been further suggested that the agerelated changes in 5-HT neurons may predispose the elderly to develop depression. There is also increasing evidence that a combination of disturbances in cholinergic and serotonergic function may play a role in cognitive impairment in Alzheimer's disease (AD), with serotonergic dysfunction potentially responsible for a significant portion of the behavioral aspects of the disease. This implication of the 5-HT system in aging and age-related cognitive and mood disorders rests in large part on post mortem studies and animal models, which are limited in their capacity to predict dynamic human biochemical-behavior relationships or to accurately model the living human brain. Initial applications of functional brian imaging with positron emission tomography (PET) in the in vivo study of the brain in aging, depression, and dementia focused on characterizing alterations in physiological measurements of cerebral metabolism and perfusion. However, recent advances in PET radiochemistry, instrumentation, and image processing have paved the way for noninvasive means to test specific hypotheses regarding the direct involvement of 5-HT neurons in the behavioralMajor depression in late life and Alzheimer's disease (AD) are disorders of enormous and increasing public health significance. The prevalence of major depression is estimated at 1% to 10% of persons 60 years of age or older, whereas depressive symptoms may occur in up to 20% (Blazer et al. 1987; Borson et al. 1986; Casey 1994). Substantially higher rates of both major and minor depressions occur among institutionalized aged persons (Parmelee et al. 1989). Furthermore, the rate of suicide in this age group is higher than at any other Address correspondence to: Carolyn Cidis Meltzer, M.D., University of Pittsburgh Medical Center, PET Facility, B-938, 200 Lothrop Street, Pittsburgh, PA 15213-2582. Received March 6, 1997 accepted October 3, 1997. 408 C.C. Meltzer et al.N EUROPSYCHOPHARMACOLOGY 1998 -VOL . 18 , NO . 6 stage of life (Casey 1994). Psychosocial issues such as bereavement, disability, and declining health may serve as contributing factors in the development of geriatric depression (Casey 1994;Gilewski et al. 1991;Kennedy et al. 1991). Ad is truly a disorder of aging, with an incidence of 5% in persons older than 65 years and doubling of disease prevalence every 5 years after age 65; affected individuals represent 20% to 50% of the population after age 80 (Cross and Gurland 1986) (Evans et al. 1989). Costs associated with dementia burden exceed $90 billion annually in the United States (Ernst and Hay 1994). Depression is commonly seen in AD patients and may further interfere with cognitive function, as well as substantially...

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Alzheimer's disease: Neurofibrillary tangles in nuclei that project to the cerebral cortex

Cited by 199 publications

References 33 publications

Plastic Neuronal Remodeling Is Impaired in Patients with Alzheimer’s Disease Carrying Apolipoprotein ε4 Allele

Plastic Neuronal Remodeling Is Impaired in Patients with Alzheimer’s Disease Carrying Apolipoprotein ε4 Allele

Selective Antibody-Induced Cholinergic Cell and Synapse Loss Produce Sustained Hippocampal and Cortical Hypometabolism with Correlated Cognitive Deficits

Serotonin in Aging, Late-Life Depression, and Alzheimer's Disease: The Emerging Role of Functional Imaging

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