An hypothesis about redundancy and reliability in the brains of higher species: Analogies with genes, internal organs, and engineering systems

Glassman, Robert B.

doi:10.1016/s0149-7634(87)80014-3

Cited by 42 publications

(32 citation statements)

References 22 publications

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“…Nonetheless, evolutionary influences on brain size appear to relate size to function (Glassman, 1987; Haug, 1987; Jerison, 1987; Pagel et al, 1988; Stern, 2002) and therefore, from a ‘brain reserve’ perspective (Satz, 1993; Stern, 2002), smaller size suggests vulnerability (Peterson et al, 2000a). Smaller brain size may also be associated with early injury, perinatal stressors and nutritional deficits and is associated with development of neuropsychiatric disorder, particularly schizophrenia (Gosch et al, 1997; Gur et al, 2000a; Gur et al, 2000b; Peterson et al, 2000a).…”

Section: Discussionmentioning

confidence: 99%

“…Within the limits of normality, the basic premise of the brain reserve hypothesis is that larger pre-morbid brain volume is protective against the development of dementia. The protective influence may be related to size-complexity and size-redundancy issues (Glassman, 1987), where a larger brain may have “reserve” capacity associated with increased complexity or redundancy (Satz, 1993; Stern, 2002; 2007). The oft cited study in support of this position is one by Katzman et al (1988) where, at post mortem, senile plaques and neurofibrillary tangles were found in sufficient numbers to make the pathological diagnosis of AD in subjects who, prior to death, did not meet clinical criteria for dementia.…”

Section: Introductionmentioning

confidence: 99%

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Intracranial volume and dementia: Some evidence in support of the cerebral reserve hypothesis

Tate¹,

Neeley²,

Norton³

et al. 2011

Brain Research

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The brain reserve hypothesis has been posited as being one important mediating factor for developing dementia, especially Alzheimer’s disease (AD). Evidence for this hypothesis is mixed though different methodologies have made these findings difficult to interpret. We examined imaging data from a large cohort (N=194) of mixed dementia patients and controls 65 yrs old and older from the Cache County, Utah Study of Memory and Aging for evidence of the brain reserve hypothesis using total intracranial volume (TICV) as a quantitative measure of premorbid brain size and a vicarious indicator of reserve. A broader spectrum of non-demented elderly control subjects from previous studies was also included for comparison (N=423). In addition, non-parametric classification and regression tree (CART) analyses were performed to model group heterogeneity and identify any subgroups of patients where TICV might be an important predictor of dementia. Parametrically, no main effect was found for TICV when predicting a dementia diagnosis, however, the CART analysis did reveal important TICV subgroups, including a sex differential wherein ε4 APOE allele presence in males and low TICV predicted AD classification. TICV, APOE, and other potential mediator/moderator variables are discussed in the context of the brain reserve hypothesis.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Intracranial volume and dementia: Some evidence in support of the cerebral reserve hypothesis

Tate¹,

Neeley²,

Norton³

et al. 2011

Brain Research

View full text Add to dashboard Cite

show abstract

“…This approach is known today as the ''brain reserve hypothesis'' (Alexander et al, 1997;Coffey et al, 1999;Fotenos et al, 2008;Jorm et al, 1997;Reynolds et al, 1999;Roe et al, 2008;Schmand et al, 1997). How a larger premorbid brain volume can protect against the development of dementia is unclear, albeit some ideas have been suggested (Glassman, 1987;Katzman et al, 1988;Stern, 2002Stern, , 2007. It is important to note that several studies did not find data to support the notion that a larger brain is protective against AD (Jack et al, 1997;Jenkins et al, 2000;Pantel et al, 1997).…”

mentioning

confidence: 99%

Intracranial volume, cranial thickness, and hyperostosis frontalis interna in the elderly

May

Mali

Dar

et al. 2012

American J Hum Biol

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HFI is accompanied by an increase in thickness of all calvarial bones and reduced ICV. In addition, the thickening process initiated by HFI is synchronized among the calvarial bones. Presence of HFI suggests a decrease in brain volume and has a major clinical significance as it may indicate the beginning of degenerative processes of the brain. In addition, as females age, their skulls tend to develop more robust characteristics.

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“…Taken together, the results of both studies indicate that when the brain is injured earlier in life it does not age as well as it would normally. One explanation that has been put forth to explain this kind of accelerated aging of the brain after injury is the ''margin-ofsafety'' model (Teuber, 1974;Glassman, 1987). This theory posits that the organization of the brain is intrinsically redundant, allowing normal functioning to be maintained despite the loss of a considerable amount of tissue.…”

Section: Discussionmentioning

confidence: 99%

Changes in dendritic morphology and spine density in motor cortex of the adult rat after stroke during infancy

Hartle

Jeffers

Ivanco

2010

Synapse

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Cognitive and motor deficits are pervasive in children that suffer early brain injury. The aim of this study was to determine the impact that early damage has on dendritic spine density and other aspects of dendritic morphology of neurons in the motor cortex. Also of interest was how changes in dendritic structure evolved across the lifespan. Ischemia was induced in 10-day-old Long Evans rats by injection of Rose Bengal dye and a laser positioned over right motor cortex. Animals were sacrificed at two and six months of age, and brains were processed for Golgi-Cox staining. Animals exposed to early damage exhibited increases in length of basilar dendrites at two months of age, however no differences in spine density were found across groups at this age. At six months of age, injured animals demonstrated an overall decrease in apical and basilar spine density. Our results suggest that the changes in dendritic length and spine density observed after early damage are unable to be maintained as the animal ages. The observation that increases in spine density do not necessarily coincide with increases in dendritic length suggests that the two processes may not be dependent on one another and suggest two independent plasticity processes responding to damage.

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An hypothesis about redundancy and reliability in the brains of higher species: Analogies with genes, internal organs, and engineering systems

Cited by 42 publications

References 22 publications

Intracranial volume and dementia: Some evidence in support of the cerebral reserve hypothesis

Intracranial volume and dementia: Some evidence in support of the cerebral reserve hypothesis

Intracranial volume, cranial thickness, and hyperostosis frontalis interna in the elderly

Changes in dendritic morphology and spine density in motor cortex of the adult rat after stroke during infancy

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