Abstract
Background It has been shown that there is an age-related decrease in CSF production in the Fischer rat brain, and that this decrease follows the CNS deposition of amyloid rather than preceding it [1]. We have postulated that amyloid and Tau accumulation in normal aging is multi-factorial, combining early defects in the blood-brain barrier (BBB) efflux transport of amyloid beta-peptide (A-beta) with later changes in CSF production and turnover, as well as up-regulation of A-beta influx transport.
Highlights
It has been shown that there is an age-related decrease in CSF production in the Fischer rat brain, and that this decrease follows the CNS deposition of amyloid rather than preceding it [1]
We have postulated that amyloid and Tau accumulation in normal aging is multi-factorial, combining early defects in the blood-brain barrier (BBB) efflux transport of amyloid beta-peptide (A-beta) with later changes in CSF production and turnover, as well as up-regulation of A-beta influx transport
HpTAU pT231 and AT-100 increased with aging by western blotting (WB) measurement: pT231 increasing nearly fourfold by age 36 mos and AT-100 doubling
Summary
It has been shown that there is an age-related decrease in CSF production in the Fischer rat brain, and that this decrease follows the CNS deposition of amyloid rather than preceding it [1]. We have postulated that amyloid and Tau accumulation in normal aging is multi-factorial, combining early defects in the blood-brain barrier (BBB) efflux transport of amyloid beta-peptide (A-beta) with later changes in CSF production and turnover, as well as up-regulation of A-beta influx transport. LRP-1 and P-gp began to decrease between nine and 12 months whereas RAGE increased significantly much later in life. CSF production increased from three to 12 mos and decreased. Mean CSF production rates were 1.8 ± 0.1 μl/ min at three mos, rising to 2.5 ± 0.2 μl/min at 12 mos (p = 0.05), falling to 2.0 ± 0.3 μl/min at 30 mos (p = 0.06)
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