There are a great many exceedingly complex and still comparatively poorly understood structures inside our cells. If you're even passingly familiar with the varied roles of mitochondrial damage or protein misfolding or the the decline of cellular housekeeping processes such as autophagy in aging, then the Golgi apparatus certainly has the look of a thing that should be more important in aging than seems to be the case. You'll find no mention of it in the Fight Aging! archives prior to today:
Cells synthesize a large number of different macromolecules. The Golgi apparatus is integral in modifying, sorting, and packaging these macromolecules for cell secretion (exocytosis) or use within the cell. It primarily modifies proteins delivered from the rough endoplasmic reticulum but is also involved in the transport of lipids around the cell, and the creation of lysosomes. In this respect it can be thought of as similar to a post office; it packages and labels items which it then sends to different parts of the cell.
Where the Golig apparatus is implicated in aging, it is in the context of Alzheimer's disease. In the brain cells of Alzheimer's patients the Golgi apparatus seems to fall apart, and researchers here suggest that this is an important step in the progression of pathological effects at the biochemical level. They identified one of the mechanisms by which the progression of Alzheimer's is sabotaging the Golgi structures, blocked it, and saw a consequent reduction in levels of the characteristic harmful amyloid beta associated with Alzheimer's disease. That is somewhat promising, even if only accomplished in cells rather than laboratory animals:
University of Michigan researchers have learned how to fix a cellular structure called the Golgi that mysteriously becomes fragmented in all Alzheimer's patients and appears to be a major cause of the disease. They say that understanding this mechanism helps decode amyloid plaque formation in the brains of Alzheimer's patients - plaque that kills cells and contributes to memory loss and other Alzheimer's symptoms.
The researchers discovered the molecular process behind Golgi fragmentation, and also developed two techniques to 'rescue' the Golgi structure. "We plan to use this as a strategy to delay the disease development. We have a better understanding of why plaque forms fast in Alzheimer's and found a way to slow down plaque formation."
Researchers found that the accumulation of the Abeta peptide - the primary culprit in forming plaques that kill cells in Alzheimer's brains - triggers Golgi fragmentation by activating an enzyme called cdk5 that modifies Golgi structural proteins such as GRASP65. [The researchers] rescued the Golgi structure in two ways: they either inhibited cdk5 or expressed a mutant of GRASP65 that cannot be modified by cdk5. Both rescue measures decreased the harmful Abeta secretion by about 80 percent. The next step is to see if Golgi fragmentation can be delayed or reversed in mice.
Some research in the Alzheimer's field suggests that amyloid levels in the brain are fairly dynamic, and thus Alzheimer's may well be a progressive failure of processes that work to clear out harmful amyloid, not a slow accumulation of unwanted compounds. If that is the case, a way to reduce the pace of creation might be enough to tip things back over into a comparatively healthy state. The only fix in the long term, however, is to identify and eliminate the root causes of the condition, whatever they might turn out to be.