Age-related dendritic growth in dentate gyrus of human brain is followed by regression in the ‘oldest old’

Flood, Dorothy G.; Buell, Stephen J.; Defiore, Charles H.; Horwitz, Gary J.; Coleman, Paul D.

doi:10.1016/0006-8993(85)91018-2

Cited by 109 publications

(40 citation statements)

References 12 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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“…Indeed, positron emission tomography (PET) studies (Chugani et al, 1987;Jacobs et al, 1995) and quantitative neuromorphological investigations (Huttenlocher, 1979(Huttenlocher, , 1990Rakic et al, 1986;Huttenlocher and de Courten, 1987;Jacobs and Scheibel, 1993) indicate that the aging pattern of cerebral metabolism closely tracks life-span histological changes. The present Golgi analysis extends previous morphological research (Buell andColeman, 1979, 1981;Flood et al, 1985;Nakamura et al, 1985;Jacobs and Scheibel, 1993;Anderson and Rutledge, 1996) by quantitatively exploring agerelated dendritic/spine changes in left frontopolar (Brodmann's area 10) and occipital (Brodmann's area 18) regions of the human neocortex (Brodmann, 1909).…”

mentioning

confidence: 81%

“…Poly-and supramodal cortical association areas, including the prefrontal cortex, appear particularly susceptible to aging, with relative sparing of sensory regions, such as the occipital cortex (Kuhl et al, 1982;Smith, 1984;Raz et al, 1993Raz et al, , 1997. Second, despite considerable research on the histological consequences (e.g., decreases in cell number) of aging in humans (Anderson et al, 1983;Terry et al, 1987), few quantitative dendritic investigations have addressed regional specificity in human aging because each study has generally focused on only one cortical area (see, e.g., Flood et al, 1985;Nakamura et al, 1985;Jacobs and Scheibel, 1993;Anderson and Rutledge, 1996). Thus, the present study is the first to examine quantitative age-related changes in human dendritic/spine systems across both areas 18 and 10.…”

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confidence: 98%

Life-span dendritic and spine changes in areas 10 and 18 of human cortex: A quantitative golgi study

Jacobs

Driscoll

Schall³

1997

J. Comp. Neurol.

365

246

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Dendritic neuropil is a sensitive indicator of the aging process and may exhibit regional cortical variations. The present study examined regional differences and age-related changes in the basilar dendrites/spines of supragranular pyramidal cells in human prefrontal (area 10) and secondary occipital (area 18) cortices. Tissue was obtained from the left hemisphere of 26 neurologically normal individuals ranging in age from 14 to 106 years (M(age) = 57 +/- 22 years; 13 males, 13 females). In tissue prepared by a modified rapid Golgi technique, ten neurons were sampled from each cortical region (N = 520) and were evaluated according to the following parameters: total dendritic length, mean segment length, dendritic segment count, dendritic spine number, and dendritic spine density. The effects of age and Brodmann areas were analyzed with a nested multiple analysis of variance design. Despite considerable interindividual variation, several clear findings emerged: 1) Dendritic systems were significantly larger in area 10 than in area 18 across the sampled life span, presumably because of the more integrative function of area 10 neurons. 2) There was a significant age effect, with a substantial decline in dendritic neuropil from the younger (< or =50 years) group to the older (>50 years) group, especially in spine measures, which decreased almost 50%. 3) Dendritic values were relatively stable after 40 years of age, suggesting that dendritic/spine degeneration in older, relatively healthy individuals may not be an inevitable consequence of the aging process. These findings underscore the importance of life-long commitment to a cognitively invigorating environment.

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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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Age-related dendritic growth in dentate gyrus of human brain is followed by regression in the ‘oldest old’

Cited by 109 publications

References 12 publications

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

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

Life-span dendritic and spine changes in areas 10 and 18 of human cortex: A quantitative golgi study

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

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