Alzheimer’s Disease and risky sexual behavior: not quite a false alarm?

Abel over at Terra Sigillata got is writ in a tinger over bad grammar and was concerned that Alzheimer’s Disease had been tied to risky sexual behavior. His conclusion was that he got a poorly worded email notice about two separate problems that were linked inappropriately by a semicolon. So everything’s fine, all clear, right? He’s free to engage in risky sexual behavior without fear of getting Alzheimer’s Disease (AD) later in life!
That’s not entirely true.
We’ve known that inflammation plays a huge role in the Alzheimer’s disease process. Unfortunately, inflammation is caused by a number of sexually transmitted diseases, such as those of the herpes family. What’s more, herpes viruses have a proclivity for neural tissue. Multiple herpes viruses have been found in the brains of AD patients; indeed (note the proper use of a semicolon, Abel), herpes simplex 1 (HSV-1) is a known risk factor for AD. Additionally, other herpes viruses have been studied and it appears that human herpes virus 6 (HHV-6) type B (but not type A) may be another with a strong link to incidence of AD. Cytomegalovirus (CMV) and HSV-2 seems to lack a relationship, and very few control or AD brains are infected with them.
Now now now, I know what you’re thinking. You’re saying “Aha Evil! HSV-2 is the simplex virus commonly associated with sexual activity!” While this is true, HSV-1 infection can and does result from sexual activity, just as HSV-2 is not only transferred via genitogenital contact. CMV is also transmitted sexually.
As I said, thankfully, HSV-2 rates seem to be quite low in AD brain and in elderly control brain. However, that could change in the future. As Tara at Aetiology mentions, the elderly are a population that is at an increasingly high risk for STD transfer, as the geriatric population is largely ignored by educational efforts, and they are less likely to practice safe sex or use condoms . An increase in the incidence of HSV-2 in the elderly could conceivably change that.
To make matters worse, those at risk for AD due to the presence of the apoE4 gene get a double whammy: HSV-1 is present at higher levels in the brains of those with the apoE4 allele, and HSV-1 shifts processing of amyloid precursor protein into Abeta (1-40) and (1-42) overdrive, which is unfortunate since Abeta protein fragments are what aggregate and form one of the pathological hallmarks of AD; the amyloid plaque. Fibrillar Abeta is thought to “gum up” synapses and contribute to neuronal dysfunction and cell death.
On a related note, CMV may also cause problems for the aging noggin– it is transmitted sexually and also increase the risk of vascular dementia.
It is thought that merely having, say, HSV-1 isn’t causative (obviously it isn’t because 85% of people have HSV-1 from a young age and not that many people develop AD), but that HSV-1 “flareups” in the brain, over time, increase the inflammatory processes that contribute to AD, so that the effect is cumulative.
So Abel, you’re sorta right and unfortunately sorta not. We don’t have rock solid evidence that sex=Alzheimer’s by a long shot, but there’s definitely some cause for concern that STDs (or at least viruses that target the brain and can be transmitted sexually) may be contributing to the incidence of AD, and quite possibly to other neurodegenerative diseases.

Promising Effects of Statins on Alzheimer’s Pathology

Finally we get some data on changes in AD pathology with statin use! Statins are taken for lowering cholesterol, but they have other beneficial effects such as modulating inflammatory responses. Thus, they could prove beneficial in the treatment of AD given the disease has a significant inflammatory component.
According to the press release

The two changes in the brain that are considered the most definitive hallmarks of Alzheimer’s are brain “plaques” and “tangles.” After controlling for variables including age at death, gender, and strokes in the brain, the researchers found significantly fewer tangles in the brains of people who had taken statins than in those who had not. “These results are exciting, novel, and have important implications for prevention strategies,” said senior co-author Eric Larson, MD, MPH, the leader of the ACT study and executive director of Group Health Center for Health Studies. “But they need to be confirmed, because ACT is not a randomized controlled trial.”

As the press release rightly points out

A randomized controlled trial of statin treatment and brain autopsy findings would be problematic for ethical and practical reasons, said Dr. Larson. But the ACT setting made the study more rigorous than previous observational epidemiological studies, because it uses reliable automated pharmacy records, is based in a community population, and includes autopsies in people both with and without dementia.

so don’t expect any prospective comparisons anytime soon. Or, ever. However, this study appears promising as it backs up the epidemiological data. I’ll have to see if I can get my hands on the actual paper and post about it.

Eat chana masala to prevent Alzheimer’s!

Yes, that title is a bit ostentatious. But the foods we eat contain many compounds that can be beneficial to brain health. One strategy for optimizing our brains for long-term peak performance is to identify these compounds and discover how they are beneficial. Head-healthy chemicals have previously been isolated from curries and spices before, and it looks like we’ve found another curcuminoid, bisdemethoxycurcumin, which may be useful in combating Alzheimer’s Disease:

Researchers have isolated bisdemethoxycurcumin, the active ingredient of curcuminoids — a natural substance found in turmeric root — that may help boost the immune system in clearing amyloid beta, a peptide that forms the plaques found in Alzheimer’s disease. Using blood samples from Alzheimer’s disease patients, researchers found that bisdemethoxycurcumin boosted immune cells called macrophages to clear amyloid beta.

The results also suggest a new drug development approach for the disease that differs from the amyloid-beta vaccine. The new approach relies on the innate immune system, which is present at birth rather than on antibodies produced by B cells, which is a later developed part of the active immune system.

I like these strategies. Chemicals that occur naturally in the diet and which have anti-inflammatory properties can be consumed in low levels, chronically, and provide health benefits on the cheap. Combining these dietary benefits with drug-based strategies may in fact boost performance of the drugs, and if nothing else we have a new chemical structure to tinker with and hopefully provide more effective therapeutic agents in the future. Additionally, anti-inflammatory dietary factors can protect other organ systems from a myriad of inflammation-related issues that occur with aging.

Thoughts on Approaching Hormone Therapy Data

I recently posted three “Basics”-style blurbs about menopause and hormone therapy (HT). If you missed it, they are here, here, and here. The field has gone through a lot of upheaval since the WHI studies in 2002, and I would just like to share my thoughts on how to approach where we stand now. These are the sorts of questions and considerations that researchers and health care professionals need to keep in mind when they evaluate HT. After the reference-heavy previous posts this one is going to just be my thoughts, and very off-the-cuff at that.
We, as humans, have a tendency to put things in conceptual boxes. Cholesterol bad. Eggs bad. No wait eggs good. Hormone therapy good. No wait hormone therapy bad. Unfortunately, endocrinology doesn’t like boxes. Hormones abhor predictability. In fact endocrinology is a frakkin’ nightmare even when you’re dealing with one simple feedback loop. So when you hear that “estrogen is bad again” in the news, STOP.

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The Basics of Menopause and Hormone Therapy III: Cognitive Consequences

This is the third part in an overview of menopause and hormone therapy. Parts one and two are here and here. This time around I describe changes in cognitive and behavioral profiles for women and animal models of menopause. I may decide to expand on a handful of studies at a later date, but for now I wanted to provide a very brief overview of human studies, problems inherent to human studies, and animal studies. I think the next part of this series will focus on the quality of our animal models and what they have to tell us. But for now, anyone who is interested in these issues knows where to start digging!
Granted, some of the info in this series is a bit dated, but I’ll do future posts to expand on recent findings. I also posted a follow-up on factors to consider when evaluating hormone therapy use and comparing new findings to “common wisdom”.

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The Basics of Menopause and Hormone Therapy II: Types of HRT and Physiological Consequences

This is the second of a series that examines menopause, hormone therapy, and consequences of each. Today’s installment looks at the makeup of common hormones on the market, physiological consequences of hormone loss and replacement, and the Women’s Health Initiative (WHI) studies. A slight emphasis is placed on Alzheimer’s Disease as a segway to the next installments, which will focus on cognitive and neurobiological consequences of menopause and hormone therapy.

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The Basics: History of Hormone Therapy and Menopause

I thought I’d hop on the Basics bandwagon. Here’s an oldy of mine with some menopause and hormone therapy background. WARNING: rampant pharmaceutical company sexism ahead. Do not attempt to communicate or reason with Zuska for at least 4 hours after reading. Rumor also has it that Tara is advocating for a beat-down.
Parts II and III are here and here.

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