Dendritic extent in human CA2–3 hippocampal pyramidal neurons in normal aging and senile dementia

Flood, Dorothy G.; Guarnaccia, Michael M.; Coleman, Paul D.

doi:10.1016/0006-8993(87)90744-x

Cited by 73 publications

(20 citation statements)

References 23 publications

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“…19] and dentate gyrus [21,29], Age-related stability in dendritic extent is also documented in human hippocam pal subfields CA1 [23], CA2/3 [30], and subiculum [20]. These findings are consistent with the trends observed in the current data and suggest that normal human aging in temporal lobe limbic structures is not accompanied by dendritic loss, but rather, increased dendritic length within this age span.…”

Section: Discussionsupporting

confidence: 82%

Dendritic Atrophy and Remodeling of Amygdaloid Neurons in Alzheimer's Disease

Scott

1993

Dement Geriatr Cogn Disord

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The current study examined changes in the dendritic arbor of basolateral amygdaloid neurons in Alzheimer's disease (AD). Quantitative analysis of Golgi Kopsch-impregnated tissue samples revealed a significant reduction in the total dendritic length per neuron in AD. Terminal and nonterminal dendritic segments were affected similarly. Somatofugal ordering of the same segments, however, indicated that the reductions were restricted to the inner portion of the dendritic tree, coupled with significant AD-related increases in the length and number of the highest order segments. These data suggest that despite an overall AD-related loss of dendritic length in this amygdaloid subregion, new dendritic segments continue to form. The loss of proximal segments, combined with the gain of distal segments, may be interpreted as dendritic remodeling in the course of the disorder.

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Section: Discussionsupporting

confidence: 82%

Dendritic Atrophy and Remodeling of Amygdaloid Neurons in Alzheimer's Disease

Scott

1993

Dement Geriatr Cogn Disord

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“…Segment length is represented on the abscissa and spine density on the ordinate. McNeil1 et al, 1990), in hippocampal neurons of aged humans (Buell and Coleman, 1981;Flood et al, 1985Flood et al, , 1987, and in striatal cells in moderate grade Huntington's disease (Graveland et al, 1985;Ferrante et al, 1991). In each of these instances, however, the effects are transient and dendritic proliferation is followed by degeneration.…”

Section: Dutu Analysis: Critique and Interpretationsmentioning

confidence: 99%

Effects of dopamine depletion on the morphology of medium spiny neurons in the shell and core of the rat nucleus accumbens

1995

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Nucleus accumbens receives a dense dopaminergic innervation which is important in regulating motivated states of behavior such as goal- directed actions, stimulus-reward associations and reinforcement of addictive substances. The shell and core territories of this nucleus each receive functionally and morphologically distinct dopaminergic inputs and lesions of the ascending pathways totally deprive the core but not the shell of dopaminergic fibers. Medium spiny neurons are the principal targets of dopaminergic terminals. The present study explored whether the loss of dopamine inputs can affect these neurons and whether cells in the shell and core would be equally susceptible to such a loss. Intracellular injection in fixed slices and neuronal reconstruction were used to analyze the dendritic trees of 62 neurons in the shell and core of animals that received a unilateral, chronic 6- hydroxydopamine lesion of the medial forebrain bundle. In the dopamine- depleted core, dendrites are significantly shorter (16% decrease) than in the intact core and in both the dopamine-depleted core and lateral shell, dendrites are less spiny than in respective control regions. Dopamine loss in the medial shell is associated with significantly more tortuous dendrites that are lower in spine density. However, the number of spines is not reduced which may mean that the increase recorded for segment length, although insignificant in tests, could be responsible for the change in spine density. These data suggest that the loss of dopamine can affect accumbal neuronal morphology and, moreover, can affect neuronal structures differentially in the shell and core.

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“…Aberrant swellings of the initial segments of axons ("meganeurites"), a feature that occurs with increasing frequency in human brains beginning at about age 50, also show a striking regional selectivity (e.g., layer III but not layer V of the frontal cortex), which matches well with the distribution of tangles (Braak, 1984). Dendritic abnormalities Flood et al, 1987), including the loss of branches and spines, associated with AD have a distribution that overlaps the tangles per se (e.g., CA1 and subiculum) or the targets (e.g. dentate granule cells) of projecting neurons that are prone to tangles (for a recent review, see Anderton et al, 1998).…”

mentioning

confidence: 98%

Spatial patterns of mammalian brain aging: Distribution of cathepsin D–immunoreactive cell bodies and dystrophic dendrites in aging dogs resembles that in Alzheimer's disease

Head

Cotman

et al. 2003

J of Comparative Neurology

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Elevated levels of the lysosomal enzyme cathepsin D are found in the early stages of Alzheimer's disease (AD) and co-occur with intraneuronal tangles. The present study tested whether increases in cathepsin D would emerge during aging in another mammalian species. Regional brain patterns of cathepsin D immunostaining were compared in dogs ages 0.35 to 16 years. Accumulations of immunopositive material were evident in neuronal cell bodies in many forebrain sites in middle-age to old dogs (>/=6 years). Three types could be distinguished: (1) dense aggregates with no particular position within the cell body; (2) crescent-shaped "caps" that occupied one pole of the cell body; and (3) very dense "spikes" that extended from the cell body for variable distances into the apical dendrite; these spikes were found in only a few areas, most notably the subiculum and layer V of neocortex. The spikes appeared between ages 2 and 5 years and increased steadily with age thereafter. Spikes were found in the subiculum in the aged human brain but only infrequently; they were, however, present in large numbers in AD brains. These results established that brain aging in dogs is (1) well advanced by middle age, (2) varies markedly across regions, and (3) in at least some of its aspects (dystrophic dendrites) is prominent in areas known to exhibit pathology early in the course of AD. Combined with previous results for rats, these findings indicated that changes in cathepsin D observed in AD, in particular in the temporal lobe, reflect a generalized mammalian pattern of brain aging.

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Dendritic extent in human CA2–3 hippocampal pyramidal neurons in normal aging and senile dementia

Cited by 73 publications

References 23 publications

Dendritic Atrophy and Remodeling of Amygdaloid Neurons in Alzheimer's Disease

Dendritic Atrophy and Remodeling of Amygdaloid Neurons in Alzheimer's Disease

Effects of dopamine depletion on the morphology of medium spiny neurons in the shell and core of the rat nucleus accumbens

Spatial patterns of mammalian brain aging: Distribution of cathepsin D–immunoreactive cell bodies and dystrophic dendrites in aging dogs resembles that in Alzheimer's disease

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