Regarding the recent reports of "transmissible Alzheimer's"

And why the role of amyloid beta proteins may be rather complex.

By now readers may have come across articles regarding the possibility that some cases of Alzheimer’s disease may be related to a therapy that was halted in the 1980’s.

Some titles include the following:

From CNN

From Nature

From BBC

From Science

These reports are based on a recent Nature Medicine study¹ from John Collinge and his team at the University College of London, in which the team has been researching possible maladies related to human growth hormone derived from cadavers (named c-hGH). This treatment was used predominately in children dealing with various health issues regarding dysfunctional/removed pituitary glands, with these cadaver-deried hGH serving as a means to provide them exogenous sources of HGH.

The practice of using c-hGH went on for several years up until the 1980s. Unfortunately, evidence seems to suggest that some vials of these cadaver-derived hormones may have been contaminated with prion-like proteins, possibly stemming from cadavers who had evidence of prion diseases such as Creutzfeldt-Jakob disease. Part of this contamination may have stemmed from negligence in using deceased individuals with possible prion pathologies, as well as due to purification methods that didn’t remove these prions. In a lot-concerned society, it appears that certain batches of c-hGH utilizing a different purification method may be responsible for the prion contamination.

Either way, the use of this contaminated c-hGH raised concerns over iatrogenic cases of CJD, and it’s believed that a few hundred cases of CJD reported worldwide may be derived from contaminated products, with many of these cases appearing in France, the UK, and the US in the years following the use of c-hGH.

Collinge’s team has worked to investigate several cases of maladies in people who have been provided c-hGH as children, and have published prior works that seem to have raised questions over the possible transmissible nature of amyloid plaques which have been associated with several forms of dementia, including a prior study in which some deceased patients with CJD also appeared to have evidence of amyloid plaques (from the Science article):

John Collinge, a neurologist at University College London (UCL), has long been interested in this form of growth hormone therapy and its occasional tragic aftermath. About 1800 people in the United Kingdom received the treatment, most as children. His team became a referral center for those who later developed concerning symptoms.

But in 2015, Collinge’s team reported a different find: Autopsies of four people who had died of CJD induced by the therapy showed their brain blood vessels were awash in beta amyloid. This caught the researchers’ attention because people with Alzheimer’s disease develop sticky beta amyloid plaques in their brains, and in many patients, this protein builds up in brain blood vessels, too. Not everyone with amyloid buildup develops dementia, however, suggesting the toxic protein may be necessary but not sufficient for Alzheimer’s to strike.

These findings seemed to have “seeded” the ground for speculations as to whether amyloid plaques may themselves transmit to individuals via iatrogenic means such as surgery with contaminated medical equipment. It also seems to have led to speculations over whether amyloid plaques themselves may act in a “prion-like” fashion as Collinge’s team conducted a study in which they took old vials of c-hGH containing amyloid beta, provided them to mice, and noticed pathologies related to dementia in these mice.

All that being said, the current findings of dementia-like disease in individuals provided c-hGH as children raises serious concerns in how this would affect medical procedures as it may suggest a possible iatrogenic method of seeding dementia in patients.

This leads to the recent research in which authors note several cases of amyloid plaques in those provided c-hGH as children.

Now, all of this is rather concerning, and it’s critical that medical agencies continue to track and conduct research in individuals provided these contaminated products.

And yet, at the same there are a few issues regarding some of the commentary surrounding this recent study.

So it’s the point of this article not to rebut the study, but to point out an issue in how studies are reported, and why context can help us get a better understanding of what may be going on.

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Within this study 8 people who were provided c-hGH were included. All individuals were provided c-hGH isolated with the Hartree-modified Wilhelmi procedure (or HWP). Evidence noted that vials of c-hGH that utilized this method were ones contaminated with prion proteins, thus raising a questions as to the correlative nature of those provided these contaminated vials and presentations of CJD or Alzheimer’s.

Out of the 8 cases the authors suggest that 5 of the individuals were referred due to symptoms of cognitive decline:

Five of these eight c-hGH recipients (Table 2; cases 2, 3, 4, 5 and 8) were referred with symptoms consistent with early-onset dementia, with progressive cognitive impairment in two or more domains severe enough to affect the performance of usual activities of daily living; in some cases, progression was rapid (Supplementary Information). Symptom onset was between the ages of 38 years and 49 years in four patients (cases 3, 4, 5 and 8) and at age 55 years in the remaining patient (case 2). In three of these five patients (cases 3, 4 and 8), a diagnosis of Alzheimer’s disease had been made before referral to the NPC; two individuals presented with typical amnestic symptoms (cases 4 and 8) and met National Institute on Aging and Alzheimer’s Association (NIA-AA) diagnostic criteria³⁰ for probable Alzheimer’s disease, and the other individual (case 3) presented with with non-amnestic (language) symptoms. The remaining two patients met NIA-AA diagnostic criteria³⁰ for probable Alzheimer’s disease with non-amnestic presentations (dysexecutive (case 2) and language (case 5)). All five cases would meet Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM V) criteria for major neurocognitive disorder due to Alzheimer’s disease³¹. Of the remaining three individuals, one had symptoms (onset aged 42 years; case 1) meeting NIA-AA criteria for mild cognitive impairment³² (predominantly affecting behavior and personality); one had subjective cognitive symptoms only (case 7); the other was asymptomatic (case 6). For those with symptoms, the latency from c-hGH exposure was three to four decades (Table 2).

What’s interesting is that, although these patients were all provided c-hGH as children, several of these patients (in the case of Case 1, Case 2, and Case 8) were diagnosed with craniopharyngioma- a highly rare but otherwise benign tumor predominately located within the suprasellar region of the brain - and were likely the reason for the c-hGH prescription as craniopharyngiomas are known to press onto the pituitary gland causing dysfunction and deficiencies in release of pituitary hormones.

*Refer to the supplemental case series for additional information on the individuals described below.

Although generally benign, craniopharyngiomas tend to have a high rate of recurrence, and in this case 3 of the patients mentioned appeared to have evidence of tumor relapse.

Case 1

A 47-year old man who was treated for craniopharyngioma when a child, was provided c-hGH, and was found dead unexpectedly in 2019:

He [Case 1] remained well until late 2014 (aged 42 years), when his vision deteriorated; he first noticed that he was unable to make sense of letters on his computer screen at work. This continued to progress, until large parts of his visual field were “greyed out”. He was found to have recurrence of his tumour, which was treated with further debulking surgery (February 2015) and stereotactic radiosurgery (April 2015), after which his vision in the right eye improved slightly. In October 2016 the vision in his right eye deteriorated again; repeat imaging in early 2017 demonstrated enhancement in the right cavernous sinus and hypothalamus, which was treated with further stereotactic radiosurgery in August 2017 with evidence of treatment response. He was additionally noted to have a progressive third nerve palsy on the right from the autumn of 2016, with a worsening ptosis evident from August 2017. In January 2019 he was noted to be bumping into things on the left, and repeat imaging demonstrated further growth of the recurrent tumour.

The case history notes changes in the deceased’s behavior and mood around this time (late 2014), although it strangely appears that the researchers did not correlate the symptom onset with the tumor.

Craniopharyngiomas are generally associated with headaches and visual impairments, with additional symptoms generally relating to brain structures that may be additionally compressed by the tumor. This includes the type of compression that the pituitary gland experiences, and the type of hormonal dysfunction that may manifest.

In the case of this patient a diagnosis of suprasellar craniopharyngiomas was made when the patient was 3 leading to treatment. The patient later had a tumor recurrence at age 5, suggesting that tumor recurrence was rather common for this individual. Treatment with c-hGH was done between 1976 and 1985, although the number of treatments, including treatments using vials of c-hGH utilizing HWP.

Consider that the main description for the change in this individual’s behavior is withdrawal from social and leisure activities due to the increasing visual impairment, likely related to the tumor. It’s also possible that changes in behavior may be related to the visual impairment as well.

And when a post-mortem examination was conducted it was suggested the craniopharyngioma may have become malignant in nature:

As the death was unexplained, a post-mortem examination was carried out locally by Her Majesty’s Coroner in order to ascertain cause of death. This was given as malignant transformation of craniopharyngioma; a small deposit of tumour was identified anterior to the midbrain, with features suggestive of (but not diagnostic for) a craniopharyngioma with malignant transformation. There was no evidence of intracerebral haemorrhage, although assessment of the brain was limited by extensive traumatic removal artefact of the brain, which included complete disruption of medial temporal lobes, the right cerebellar hemisphere and left occipital lobe.

Assessment of the brain noted various regions in which amyloid plaques and tangles were recognized, although tau and prion protein pathologies seemed absent.

So this raises a question of how to interpret these findings. Are these pathologies related to the c-hGH this patient was provided when younger, or is there more going on here that makes assessment of the information more complicated?

When looking at Case 2 we can notice a rather complex history, in which it appears that symptom onset was rather quick, with a noticeable decrease in visual acuity for this individual.

Case 2

A 55-year old who, in 2016, began developing rapid decline in mood and memory, with deterioration resulting in her passing 18 months post-symptom onset:

A 55-year-old woman (2016) developed new onset behavioural change, confusion and ataxia. This first manifested when she failed to collect her usual prescriptions from her family doctor, and her family found that she could become aggressive and 3 argumentative for no obvious reason. Two months after this started, she was admitted to hospital with a suspected Addisonian crisis, at which point her confusion had worsened. She was discharged home but readmitted shortly afterwards with confusion, intermittent drowsiness and deterioration in her mobility. In the months after this, she experienced a steady deterioration in her memory and gait, which became increasingly unsteady. She also developed visual hallucinations, some of which were complex (a dead cousin; a fruit machine) and odd beliefs, for example that she had attended a party and been on holiday, when this was not the case. Clinical examination identified significant visual impairment with limited upgaze, a mild left-sided hemiparesis associated with brisk reflexes and an extensor plantar on that side, all of which were longstanding. Her gait was noted to be ataxic, and she was disoriented in time and place.

Again, this individual was treated for suprasellar cranionpharyngioma at age 5, with evidence noting tumor recurrence as well at various times through this person’s life:

CT imaging aged 21 (1982) showed evidence of tumour recurrence, but not to the extent that surgical intervention was necessary. Aged 28 years (1989) she developed drowsiness and ataxia and was found to have papilloedema; CT imaging is reported as showing further tumour progression, for which she had another subtotal resection and later a ventriculo-peritoneal shunt. Three years later (1992), aged 31 years, her vision deteriorated again and an MRI confirmed further tumour recurrence, which was managed non-operatively with radiotherapy. She had to stop working as a nurse shortly after this, due to visual impairment and a left sided hemiparesis. She lived independently, and shared a home with her parents.

At this point note that several symptom overlaps have been reported, including ataxia and hemiparesis (weakness on one side of the body) both during the tumor recurrence as well as during the initial reporting of symptom onset.

Treatment with c-hGH occurred between the ages of 11-17 (1973-1978), including HWP batches, although once again the number of treatments is not provided.

Again, there doesn’t appear to be a correlation made between the symptom onset and possible tumor recurrence. And yet, a post-mortem examination noted diffuse calcified craniopharyngioma:

Brain restricted post-mortem examination (Extended Data Figure 1) demonstrated an extensively calcified craniopharyngioma with widespread invasion into surrounding brain tissue.

And again, tau pathology appeared limited to specific regions of the brain, with amyloid pathologies being recognized only within neocortex regions of the brain:

Analysis of neocortical areas included left frontal (superior and middle frontal gyri), temporal (superior and middle temporal gyri), parietal (superior and inferior parietal lobules) and occipital (striate and peristriate) cortical regions. Amyloid-β pathology in the form of diffuse deposits with patchy distribution was restricted to the neocortex (Thal phase 1, CERAD score 0). Detailed examination of the brain showed no further evidence of amyloid angiopathy in the cerebral or cerebellar parenchyma or leptomeninges. Hyperphosphorylated tau pathology in addition to exceedingly rare isolated dystrophic deposits in the cortex, was restricted to rare neurofibrillary tangles and pre-tangles, and very rare threads in the entorhinal cortex. This limited tau pathology would not meet the requirements for Braak stage 1. There was no evidence of disease-related prion protein, TDP43 or α-synuclein pathology or any other specific pathology.

The case report doesn’t make mention of recognition of the tumor during the time of rapid deterioration and hospitalization, so the association between this individual’s death and the tumor is left ambiguous, even though it raises questions as to what led to her unfortunate death. The rapid progression raises questions over the role of amyloid plaques or even prion proteins, but given lack of evidence of the latter it would be hard to argue a CJD-like role. The ambiguous nature of the amyloid plaques themselves also raise questions over the rather rapid decline.

But once again, the case here is made complex due to the actual limited nature of the amyloid plaques. Again, we have to ask the question of whether these case reports are clear evidence of amyloid pathologies associated with the c-hGH treatments, or whether some other factors should be considered.

Case 3

Unfortunately, Case 8 remains the most ambiguous of the 3 craniopharyngioma patients:

A 48-year-old man developed subtle symptoms of poor memory and cognitive slowing. These gradually progressed, and he lost his job approximately two years after these symptoms first occurred, likely as a consequence of his cognitive symptoms. At around this time, he was admitted to hospital after becoming seriously unwell with an Addisonian crisis and sepsis, and his memory difficulties significantly worsened after this period of ill health. These continued to progress over the following three years, and have particularly declined in the past year (approximately five years after these symptoms were first noticed). He is frequently confused over times and dates, and can misremember situations; examples include thinking he is late for interviews which are not scheduled, and believing that his deceased mother is still alive. He has occasionally mistaken his wife for his sister, and often asks questions repetitively. He has also lost interest in activities he previously enjoyed, such as golf, and he is eating more sweet foods than previously.

This patient was still alive at the time of reporting, and in this case the individual was diagnosed with craniopharyngioma at age 6, with c-hGH treatment occurring between the ages of 9-15 (1979-1985) including some HWP batches.

There is no mention of tumor recurrence, and evidence of residual tumor was made after a CT scan was conducted:

CSF analyses demonstrated a slightly reduced amyloid-β 1-42/1-40 ratio (0.062; values less than 0.065 suggestive of abnormal amyloid-β deposition); CSF tau was in the normal range. PrP RT-QuIC was negative. EEG was within normal limits; CT imaging of the head demonstrated stable appearances compared to the prior scan completed two years previously with evidence of a previous right frontal craniotomy and associated right frontal atrophy, residual calcified suprasellar tumour, calcification of the basal ganglia bilaterally and diffuse cerebellar atrophy. Repeat CSF testing, performed approximately 18 months after the previous lumbar puncture, showed an amyloid-β 1-42/1-40 ratio of 0.083, total tau 295 pg/mL (normal range 146 to 595 pg/mL) and phospho-tau 181 level of 43 pg/mL (normal range 0 - 58 pg/mL).

The case report doesn’t mention the time of the first lumbar puncture, although it’s strange that the amyloid-beta ratio improved at the time of the second puncture, with CSF analysis of tau proteins appearing within the normal range.

This patient was considered to be one of two confirmed diagnoses of Alzheimer’s prior to study inclusion:

Two patients clinically diagnosed with Alzheimer’s disease before our review—one amnestic (case 8) and one non-amnestic (case 3)—had biomarker changes compatible with the diagnosis, meeting the amyloid/tau/neurodegeneration, or AT(N), criteria for disorders within the Alzheimer’s continuum (Fig. 1 and Table 2)³².

It’s hard to make out exactly what the role of these tumors are for these individuals, and yet in the same ways that the authors suggest a correlation between c-hGH treatment and these possible cases of Alzheimer’s it may be worth considering an association between these tumors and the presentation of amyloid pathologies.

Unfortunately, the researchers don’t make mention of the role of tumors and the symptom onset showcased here:

The c-hGH recipients that we report here have developed new and progressive disturbances of cognition that meet standard definitions for dementia (five cases) or mild cognitive impairment (one case); they also show changes consistent with Alzheimer’s disease (definite in four cases; suggestive in two patients with a clinical diagnosis of dementia). Their relatively young age makes sporadic Alzheimer’s disease unlikely^37,38, and, as inherited causes have been excluded, we considered that their symptoms and biomarker findings are a consequence of Aβ transmission from contaminated c-hGH received in childhood. Iatrogenic Aβ transmission has resulted in human disease on several occasions, with iatrogenic CAA now a recognized cause of early-onset stroke²⁶, and the individuals whom we describe in this report have received c-hGH batches that contain quantifiable Aβ and can be used to transmit Aβ experimentally in a new host¹².

More strikingly, when the authors consider alternative hypotheses for the supposed manifestation of Alzheimer’s there doesn’t appear to be any mention of the craniopharyngioma, and instead a consideration was made for the radiotherapy:

Finally, we considered the effect of cranial radiotherapy, which was used as a treatment in four of the patients whom we describe. Radiotherapy treatment in adults with primary and metastatic brain tumors has been associated with mild cognitive impairment and dementia⁴⁷, although not Alzheimer’s disease specifically⁴⁸; data on adult survivors of childhood brain tumors are limited⁴⁹. We identified one postmortem study⁵⁰ reporting increased Aβ deposition in adults of equivalent age (30–59 years) with adult-onset malignancy (extracranial primary tumors) but without dementia. In the series of patients that we describe here, Aβ deposition was more marked in those treated with radiotherapy. However, we do not consider it plausible that radiotherapy can explain our findings. Aβ deposition after radiotherapy is likely a response to acute radiation injury; a similar process occurs after traumatic brain injury^51,52 in which Aβ rapidly accumulates in the acute phase and then clears over a period of days^53,54,55,56. Data from the above report⁵⁰ show that the mean survival time to death in individuals with Aβ deposition (70 d; range, 10–180 d) is shorter than that in the group without Aβ deposition (120 d; range, 30–300 d). This finding supports the argument that Aβ deposits after radiotherapy are cleared with time, as is the case in traumatic brain injury, although there are no specific data to confirm or refute this hypothesis.

Remember that absence of evidence is not evidence of absence. In this case, tumors were not considered as an alternative explanation for the amyloid pathologies.

This, of course, begs the question- are tumors associated with amyloid beta plaque formation?

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Tumors and amyloid beta- more connected than previously thought

It’s been well-known that various cancers are associated with the formation of amyloid-like fibrils- a phenomenon known as amyloidosis. However, many of these amyloids usually manifest within the form of aggregate immunoglobulin light chains called immunoglobulin light‐chain amyloidosis, or AL.

However, what’s interesting is that current research has noted that amyloid-beta may also be associated with cancer. For instance, research into breast cancer has noted that amyloid beta as well as amyloid precursor proteins are associated with cancer progression and proliferation.² In mouse models amyloid beta formations were found near blood vessels in mouse xenografts with inflammatory breast cancers.³ And in epidemiological investigations it was noted that elevated levels of amyloid beta were recognized in people with prior reports of cancer, and may be associated with higher risk of cancer progression.⁴,⁵

More fascinatingly, there seems to be an inverse correlation between Alzheimer’s and cancer, in which it appears that certain cancers were associated with lower rates of Alzheimer’s⁶, although such correlations should be taken from the perspective that Alzheimer’s is an age-related disease and therefore will be heavily influenced by selection bias.

So what exactly is the reason for elevated amyloid plaques in cancer? Is it that cancer itself is involved with amyloid beta formation in order to increase survivability, or is the presence of amyloid plaques due to some other reason?

What’s interesting is that amyloid beta may show anticancer properties, in which it is argued that amyloid betas may help to arrest cell development at certain points during the cell cycle.⁷ This makes the presence of amyloid beta more complex. That is, do cells release amyloid beta as a defense mechanism against cancerous cells, or do cancerous cells produce amyloid beta as a protective mechanism for themselves.

So why, then, are amyloid beta associated with neurodegeneration? The answer may lie in the cell type and the target of amyloid beta destruction, as amyloid beta may alter neuron activity and cause cellular destruction. In this case, the mechanism may be the same, but the cell type targeted may be responsible for the pathologies that become present. That is, even if amyloid beta serves a defensive role their presence within the brain may be destructive to neurons.

It’s been suggested that brain cancers are associated with symptoms similar to dementia, in which case it appears that memory loss may be due to changes in the microenvironment caused by the cancer. This may be related to amyloid beta formation, but other factors are likely at play as well.⁸

Of course, a word of caution is needed when considering this hypothesis. There are some suggestions arguing that a positive correlation exists between Alzheimer’s and cancer. The actual role of amyloid beta is also unknown.

Nonetheless, what all of this suggests is that there appears to be some relationship between tumors and the presence of amyloid beta. Whatever the relationship is, it suggests that in the case of several of the reports provided by Collinge, et al. the presence of amyloid beta may not be separable from the craniopharyngioma. That is, as much as the researchers make a claim of an association between contaminated c-hGH treatment and the presentation of Alzheimer’s, it’s clear that other factors need to be considered, and points out why the findings are more nuanced and complex than is being reported by the media.

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This is a long way to get to a conclusion that there’s more going on that what Collinge, et al. has reported, and I wouldn’t be surprised if several readers see this as a fruitless endeavor.

At the same time, how many reports of the Collinge, et al. have taken to heart the comments made by Collinge, et al. without considering alternative explanations?

Note that the c-hGH contamination is a serious case of medical malfeasance, and it’s rather important that research continues to examine correlations between those provided these treatments and possible neurological issues.

That being said, it doesn’t necessarily mean that Collinge, et al. was able to reach their “transmissible” conclusion given the fact that there are other factors that need to be worth considering. In this case, the association between cancer and amyloid beta raises a question as to whether the recognition of amyloid beta may be associated with the tumors rather than the c-hGH. This hypothesis itself warrants scrutiny, but again the point here is to suggest that it’s not so clear that a transmissible explanation can be made for the cases presented above. It’s made even worse given the time between treatment and symptom onset.

This adds to the fact that amyloid beta play more nuanced roles than previously thought, and may themselves be an antimicrobial artifact as reported by Brian Mowrey several months ago:

It's Probably Not an Alzheimer's Virus

All of this points out why it’s important to consider the context in which we are presented information, and why research should be examined with consideration for multiple factors rather than those which may support our hypothesis.

It may be evident that amyloid may be transmissible or even prion-like with further research, but for the time being this wouldn’t be the study to confirm such a hypothesis.

In summary, it’s obvious that a necessary and thorough clinical investigation should be underway to examine the extent of possible contamination and harms caused by these treatments. In the meantime, if I were to consider an iatrogenic role of amyloid beta transmissibility this probably wouldn’t be the study to look at for the time being.

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2. Lim, S., Yoo, B.K., Kim, HS. et al. Amyloid-β precursor protein promotes cell proliferation and motility of advanced breast cancer. BMC Cancer 14, 928 (2014). https://doi.org/10.1186/1471-2407-14-928

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6. Majd, S., Power, J., & Majd, Z. (2019). Alzheimer's Disease and Cancer: When Two Monsters Cannot Be Together. Frontiers in neuroscience, 13, 155. https://doi.org/10.3389/fnins.2019.00155

7. Pavliukeviciene, B., Zentelyte, A., Jankunec, M., Valiuliene, G., Talaikis, M., Navakauskiene, R., Niaura, G., & Valincius, G. (2019). Amyloid β oligomers inhibit growth of human cancer cells. PloS one, 14(9), e0221563. https://doi.org/10.1371/journal.pone.0221563

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