The relevant finding for neuroscience was the abrupt change in personal and functional ability. Not unlike the decline in cognition experienced in Alzheimer's disease--it seems to also portray the heterogeneity of not only dementia but brain injury as well. Phineas Gage may have regained a degree of normalcy and routine in his life. It made me think that although Alzheimer's disease diminishes cognition there are many patients where poor ambulation is the profound symptom--or language processing. A recent podcast, Two Scientists Walk into A Bar, examines The Degenerating Brain. Genentech brilliantly produces the podcast and surprisingly Geoff Kerchner, Neurologist and Medical Director of Early Clinical Development at Genentech is one of the first industry experts to discuss the brain in a matter-of-fact informative discussion. He is both a practicing neurologist AND a research scientist. I think this makes all the difference.
Modern neuroscientific knowledge makes the idea of Gage’s recovery all the more plausible. Neuroscientists once believed that brain lesions caused permanent deficits: Once lost, a faculty never returned. More and more, though, they recognize that the adult brain can relearn lost skills. This ability to change, called brain plasticity, remains somewhat mysterious, and it happens achingly slowly. But the bottom line is that the brain can recover lost functions in certain circumstances.--Slate
Because we are bombarded by media accounts of amyloid deposits in the brain being the potentially causative agent in Alzheimer's disease we may fail to see the forest through the proverbial "tangled and globby" trees.
Neurodegenerative diseases all seem to have a protein problem. Alzheimer's has tau and amyloid--not to be outdone, frontotemporal dementia is known for TDP-43 (also in ALS), and Parkinson's disease α-synuclein. All present in some capacity in the "normal" brain as well.
No surprise that the brain is the least understood organ of the body. The interconnectivity alone is vastly complex. Experiential influencers transmit to neurons as well. Research has demonstrated this by studying the brain of multi linguists musicians and creatives, as well as other "active" disciplines. So we do crosswords, learn foreign languages, and enjoy music when time allows. Clearly AD does not look the same in all individuals. Geoff Kerchner, MD PhD shares how common themes like memory loss are seen in many of his patients although other patients report visual spatial and navigation impairment as the most profound symptom. He reminds us that aggregating proteins is what our brain does when it is assaulted. Who is to say which of the proteins is actually driving the dysfunction?