The New York Times has a fantastic article on the neuroscience of Alzheimer’s disease, as well as the human impact of the disorder on individuals and their families.
The article is accompanied by two video reports that weave together personal stories with some of the latest developments in understanding the disorder.
Alzheimer’s is a form of dementia, which is where the mind and brain break down quicker than would be expected through normal ageing.
Like many forms of dementia, the first symptoms (such as memory, attention, language or movement problems) appear after a significant amount of brain damage has already been done.
One of the key aims of dementia research is to identify this process while it is still ‘silent’ to understand how it forms and try and prevent it developing further.
Genetics are one focus, but they are known to be complex. Certain genes (most famously ‘ApoE’) are known to alter the risk of developing the Alzheimer’s in older people, but they’re only one part of the puzzle.
However, there is one form of Alzheimer’s that is inherited in an autosomal dominant pattern, meaning that if one of your parents has it, you’ve got a fifty percent change of getting it too.
It means that if you’ve inherited the gene or genes (autosomal dominance implies a single gene, but several are currently candidates), you’re almost definitely going to develop the disorder.
Interestingly, this autosomal dominant version of Alzheimer’s tends to happen much earlier in life, in the early 60s, 50s or in some cases, even the 40s.
A similar thing happens with other similarly inherited dementias, like CADASIL, where a single gene has been fairly confidently identified.
It’s both terrifying and amazing to think that a difference in a single gene, expressing a single different protein, can cause such as massive break down in brain function.
The article also looks at a new type of dye which allows abnormal clumps of amyloid protein, a brain change characteristic of Alzheimer’s, to be seen on a PET brain scan done on living people.
At the moment, Alzheimer’s can only be diagnosed with 100% accuracy after death, but this new technique could allow brain changes to be tracked in people before they develop any symptoms.
However, it’s become clear that you can have protein clumps without having the disease.
Researchers are increasingly talking about ‘cognitive reserve‘, a measure of ‘wear and tear’ or ‘fitness’ of the brain, with the idea that the disease happens where various factors tip the brain ‘over the threshold’ into physical decline.
The ‘threshold’ is thought to be set by a combination of genetics, physical health, cognitive ability, education and level of activity.
The New York Times article is a wonderful guide to the scientific debates behind the quest to understand the disorder, and the videos really bring home the effect of it.
Link to NYT article ‘Finding Alzheimer‚Äôs Before a Mind Fails’ with videos.
Mind Hacks 
The genetics of this condition are rather troublesome, particularly to someone like me who has a family history of dementia. However, like you say, we are slowly discovering how it works, and I know science has recently uncovered the condition MCI, a kind of pre-dementia state, which is in itself an amazing find. Catching it early makes the odds of winning the fight better. You also mentioned brain “fitness,” which has been getting a lot of press lately — PBS recently aired a broadcast about neuroplasticity, the brain that changes itself ‚Äì ‚ÄúThe Brain Fitness Program,‚Äù
I think it was called. I had heard of Dr. Merzenich and his company, Posit Science, before for their breakthroughs (one of their programs was offered as a pledge gift), but it was interesting to see it all spelled out. I wouldn’t be surprised to see neuroplasticity and brain fitness methods eventually tackling some of these conditions, as we learn more. Thanks for that link, too.