Data on Brain Aging and Early Signs of Alzheimer's Disease

The brain is impacted by the processes of degenerative aging for decades before the damage rises to noticeable levels. When the technologies exist to repair this damage, treatments should ideally begin in the middle of life, not wait until there are obvious signs of degeneration. Prevention beforehand is better than restoration after the fact, for all that most of us are, at best, going to forced along the restoration route given the prospective timelines for the development of repair therapies:

Typical cognitive aging may be defined as age-associated changes in cognitive performance in individuals free of dementia. To assess brain imaging findings associated with typical aging, the full adult age spectrum should be included. Researchers compared age, sex and APOE ɛ4 effects on memory, brain structure (as measured by adjusted hippocampal volume, HVa) and amyloid [brain plaques associated with Alzheimer disease] positron emission tomography (PET) in 1,246 cognitively normal individuals between the ages of 30 and 95.

Overall memory worsened from age 30 through the 90s. HVa worsened gradually from age 30 to the mid-60s and more steeply after that with advancing age. Median amyloid accumulation seen on PET scans was low until age 70 but increased after that. Memory was worse in men than women overall, especially after 40. The HVa was lower in men than women overall, especially after 60. For both males and females, memory performance and HVa were not different by APOE ɛ4 carrier status at any age. From age 70 onward, APOE ɛ4 carriers had greater median amyloid accumulation seen on PET scans than noncarriers.The ages at which 10 percent of the population was "amyloid PET positive" were 57 years for APOE ɛ4 carriers and 64 years for noncarriers. Amyloid PET positive indicates individuals are accumulating amyloid in their brain as seen on PET scans and, while they may be asymptomatic, they are at risk for Alzheimer disease.

"Our findings are consistent with a model of late-onset AD [Alzheimer disease] in which β-amyloidosis arises later in life on a background of preexisting structural and cognitive decline that is associated with aging and not with β-amyloid deposits."



I wonder about the role of oxidized cholesterol and the atherosclerotic disease process in the early phase of cognitive decline (esp. since some degree of oxidized cholesterol accumulation can be found even in the young). I also wonder about the role of age-related systemic factors in dialing down neurogenesis in the hippocampus.

Posted by: José at March 18th, 2015 10:39 AM
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