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The Alzheimer Conundrum by Margaret Lock

1.     14 hours

2.     Recommended with reservations. I like that the author did a ton of interviews and explained things in a way that was pretty accessible for someone without a background in medicine.

3.     How I chose it: This was the most academic-looking book about Alzheimer's disease on Audible. I wanted to learn about Alzheimer's Disease because I was learning about it for work.

4.     What it is: Margaret Lock works on social studies of medicine. She interviewed a lot of AD experts and people with AD. She talked about what's going on in AD research. She talked about the politics of AD, such as how pitching and fundraising go.

5.     Full notes here.

 

AD label may be fragmented into subtaxa (but probably not for fundraising purposes!). (Chapter 1, 16  min)

 

Lots of people with amyloid plaques continue to be cognitively in good health. (Chapter 1, 25 min)

 

Many people with abnormal biomarkers don’t convert to AD, maybe 30% or so (figure highly uncertain). (Chapter 1, 35 min)

 

Is AD really isolable from wear and tear of aging? Author suggests it is an open question. (Ch 1, 36 min)

 

Amyloid plaque has been the target of most drug development (Ch 1, 40 min)

 

Incidence of dementia among people >90 yrs does not increase? [not clear on claim](Ch 1, 1:06)

 

Thomas McKeown argued that rise in human population was due to social and political factors, not improved medical care. Public health measures (like food, water, sanitation) did the trick, he says. (Ch 1, 1:07)

 

Author claims that decreasing resources allotted are being allotted healthcare in most parts of the world. This is a really not true in the US, though I know less about other places. (Ch 1, 1:12)

 

Author interviewed someone who says consolidating AD as "one condition" is just a ploy to get more funding. (Ch 2, 53 min)

 

Many researchers put energy into unraveling molecular pathways. Author claims that basic research receives the bulk of funding. Advocacy groups try to make it seem like a cure is around the corner, but no cure is in sight. (Ch 2, 1:22)

 

AD is a diagnosis of exclusion—a wastebasket category. Its what you get when you rule out lots of other conditions. (Ch 3, 17 min)

 

The dementia concept is rocky for old people. Question is whether people are normal for their age. Hard to say what the normal baseline is. (Ch 3, 28 min)

 

One interviewee: We don't really know how to separate Alzheimer's out from normal aging. (Ch 3, 42 min)

 

Characterization of amyloid cascade hypothesis. (Ch 3, 49 min)

 

Animals with massive doses of amyloid beta don't replicate the full range of AD pathology in humans. Number of amyloid plaques in the brain does not correlate well with the degree of cognitive impairment. Drug development targeting amyloid beta hasn't been successful. (Ch 3, 53 min)

 

Mark Smith suggested that amyloid should be understood as scar tissue. He thought they were not a cause of AD, but an effect of dealing with other problems. (Ch 3, 1:02)

 

Interviewee: Suggestion that plaques are sequestering amyloid beta away, keeping it away from synapses. (Ch 3, 1:06)

 

Interviewee: Aging is inextricably interwoven. Not clear what is unique to AD, a strong aging influence. If you live to 120, won't everyone get it? (Ch 4, 23 min)

 

Letter: Guy argues that amyloid is not the real cause. (Ch 5, 6 min)

 

100% of people with a certain biomarker progressed to AD over 5 years, in one study. I think this was a particular type of CSF biomarker. (Ch 5, 45 min)

 

20-40% of healthy people have plaque in their brains. It can take 10+ years for cognitive decline to happen. (Ch 5, 55 min)

 

FBP PET imaging can identify beta amyloid in the brains of living people. (Ch 5, 1:01)

 

For familial AD, age of onset can vary by as much as 10 years. Suggests environmental factors matter. 230 known mutations of APP, presenilin 1, and presenilin 2 account for 5-10% of all AD cases. (Ch 6, 7 min)

 

Sample of 1700 individuals found measurable cognitive decline as early as age 35. (Ch 6, 35 min)

 

Deposition of aBeta does not correlate well with neurofibrillary tangles, cell loss, or dementia. People suggest, instead, that aBeta is a trigger for other problems. An idea is that we should do large natural history studies with young, healthy people that are tested for years. Would be really expensive, would be beyond the reach of a pharmaceutical company. (Ch 6, 1:25)

 

I found this a bit unreasonable: "it is tempting to think that having one's genes named by an expert will bring about greater insight into future probabilities than do fables told by fortune tellers." Compares genomics to divination… (Ch 8, 2 min)

 

Amyloid plaque deposition can occur many years before symptoms. Such changes were detected up to 20 years before any symptoms. Supports the idea that we can do really early detection. (Ch 9, 38 min)

 

Research shoes that variants of "trem 2" are associated with risk for AD. (Ch 9, 1:15)

 

People generally assume that in cases where people have biomarkers for AD but don't get symptoms, the people would have gotten AD symptoms if they had lived long enough. (Ch 10, 2 min)

 

 

 

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