TY - JOUR
T1 - The aging brain
T2 - Morphomolecular senescence of cortical circuits
AU - Hof, Patrick R.
AU - Morrison, John H.
N1 - Funding Information:
We are grateful to all of our colleagues and members of the Hof and Morrison laboratories who have been involved in our studies of brain aging for their support. L. Pradier (Aventis Pharma SA, Paris, France) kindly provided access to materials from APP/PS1 M146L transgenic mice. This work was supported by NIH grants AG02219, AG05138, AG06647 and AG16765.
PY - 2004/10
Y1 - 2004/10
N2 - The human brain is uniquely powerful with respect to cognitive abilities, yet the hippocampal and neocortical circuits that mediate such complex functions are highly vulnerable to aging. Their selective vulnerability is profoundly manifested in Alzheimer's disease (AD), where degeneration of select neurons leads to a near complete loss of cognitive abilities. Most of us will avoid AD as we age. However, many will experience age-associated cognitive impairment - a decline in cognitive status presenting as deficits in memory and key capacities for strategic use of acquired information. Animal studies suggest that both AD and age-associated cognitive impairment reflect vulnerability of the same circuits. However, neuron death predominates in the former, whereas the latter is probably mediated by synaptic alterations in otherwise intact circuits. Fortunately, such age-related synaptic alterations could be reversible, as suggested by recent studies of hormone replacement.
AB - The human brain is uniquely powerful with respect to cognitive abilities, yet the hippocampal and neocortical circuits that mediate such complex functions are highly vulnerable to aging. Their selective vulnerability is profoundly manifested in Alzheimer's disease (AD), where degeneration of select neurons leads to a near complete loss of cognitive abilities. Most of us will avoid AD as we age. However, many will experience age-associated cognitive impairment - a decline in cognitive status presenting as deficits in memory and key capacities for strategic use of acquired information. Animal studies suggest that both AD and age-associated cognitive impairment reflect vulnerability of the same circuits. However, neuron death predominates in the former, whereas the latter is probably mediated by synaptic alterations in otherwise intact circuits. Fortunately, such age-related synaptic alterations could be reversible, as suggested by recent studies of hormone replacement.
UR - http://www.scopus.com/inward/record.url?scp=4544322402&partnerID=8YFLogxK
U2 - 10.1016/j.tins.2004.07.013
DO - 10.1016/j.tins.2004.07.013
M3 - Review article
C2 - 15374672
AN - SCOPUS:4544322402
SN - 0166-2236
VL - 27
SP - 607
EP - 613
JO - Trends in Neurosciences
JF - Trends in Neurosciences
IS - 10
ER -