Assets Needed or NOT Needed for Long-Term Care Are Confusing!

Read this article carefully about how to qualify for Medicaid to assist with long-term care facility costs- it’s counterintuitive!

“When you apply for Medicaid to assist with the cost of in-home care or a long stay at a nursing home facility, federal rules require you to supply five years of financial records. Large bank withdrawals made during that five-year period will send up red flags, as will setting up a trust to shelter assets or selling a home to a relative at a discounted rate.”

Caregiver Advocating

Thanks, Bruce Rhodes, for these pieces that help us get the word out about FTD and support needed:

Tips for Caregivers from Other Caregivers

Thank you to all the folks who took the time to approach me after this morning’s presentations to share their experience for your benefit. Here are some pearls, with the disclaimer that I am quoting experiences that I will take into consideration in my further practice. I have not got any scientific evidence to explain or support these reports:

  • Although I say that anti-epileptic drugs such as valproic acid or Divalproex have come into and out of vogue (then back in again) as efficacious in behavioural control, FOUR caregivers scurried up to me to report really remarkable changes for the better in their patients who were put onto valproic acid.
  • One caregiver decided to make changes in their daily diets, to see how much she could optimize her patient’s function. There is a lot of evidence to support these sorts of changes to prevent dementia, but less evidence to bolster the institution of dietary restrictions once dementia has already been diagnosed. She noted much better cognition/behavior after cutting back on foods with high or any sugar, high fat foods and caffeine. But this point will interest those looking for some control over hypersexual behavior, she believes those supplements that can enhance bloodflow (vitamin E, aspirin, and “coenzyme Q10″) maintained his abnormal libido. Another way of saying that is that withholding these agents remedied abnormal HYPERsexuality. I put coenzyme Q10in quotes above just because I do need to add disclaimer that this supplement is not known widely or prescribed for blood-thinning purposes. But there’s the advice, please do comment below so that other caregivers can get a survey of whether your experience has been similar or different.
  • Day 2 of FTD Conf

    New things I learned:

    A new presentation of FTD:

  • A new variant of primary progressive aphasia (PPA) was described, called the agnosia variant. In this form, instead of missing the meaning of words (semantic dementia or semantic variant), the patient mainly has difficulty recognizing faces. Your clinician may be the one who can help tell the difference between “I know this person but can’t remember his name” and “Who is that person you’ve been talking to for the last half hour?” Not coming up with the right name is something many of us do under certain circumstances. Semantic dementia may make this a widespread problem. The agnosia variant is the one who can’t recognize whether a face is familiar and therefore is even further from putting the right name on the person. The agnosia variant’s brain has been affected in the same area (temporal lobe) as the semantic variant, but on the right side of the brain instead of left.


  • Imaging can pick up subtle loss of volume 10 years before any change in behavior or language. The study was done on asymptomatic carriers of known genetic mutations. This may allow for the earliest testing of preventive therapies (yet to be developed).


  • I’d never thought to put it this way before, but genetics counselor Emily Dwosh at UBC pointed out that regardless of the variant of FTD diagnosed, there are both sporadic and familial cases described. This means that genetic testing may be indicated for individuals among all types of FTD presentation, even semantic dementia. In semantic dementia, we haven’t found a “culprit” genetic mutation yet, but there have been cases of multiple family members affected by the same aphasia.
  • It can take the genetics team a year to gather all the important medical records for family members affected across a few generations to determine whether the occurrence of FTD was sporadic within the context of multiple causes for dementia within the family vs. shared among all affected family members, which then makes it familial.
  • Clarification about numbers: 20% of FTD cases have a known genetic mutations. This is more than 4 X the number of Alzheimer’s disease cases with a known genetic mutation. 50% of FAMILIAL FTD cases have known genetic mutations. This explains why genetics clinics might not advise that you pursue the testing unless you are describing familial FTD.
  • At this point in clinical knowledge, if there are patients with ALS and patients with FTD in a given family, C9orf72 mutations would be more likely than progranulin mutations. This is new.
  • Genetic testing for the 3 most common mutations related to FTD could cost you $250-1200 out of pocket to order in Canada.
  • Important reminder: a negative test results does not rule out the possibility of familial FTD. The negative test result means that the family does not carry the most common mutations.
  • Some patients with FTD due to known mutations have a mild presentation of illness that lingers for 20 years, so having a mutation does not mean rapid progression or more severe illness course.

    Progress in Clinical Trials:

  • There are 53 clinical trials registered on that are recruiting patients with FTD! This has got to be an all-time high.
  • The stimulant dextroamphetamine did not help in bvFTD, semantic dementia or other PPA.
  • Oxytocin preliminary results remain positive – keep checking for this by googling “oxytocin AND FTD.”
  • Anti-tau interventions with davenutide and tideglusib have both had negative results.
  • One more anti-tau intervention, TRx0237, is still in progress. This molecule is a relative of methylene blue, which works great in the test tube against abnormally aggregating tau, but which is not itself tolerable for human use.
  • New vaccines against the Alzheimer’s disease-type of abnormal tau are in testing. If they work for Alzheimer’s patients, it would be logical to try them in FTD as well!
  • International Society for Frontotemporal Dementia Conference – Vancouver

    IMG_0729.JPGThe bi-annual international conference on FTD that features content for both scientist/clinicians and caregivers has begun again.

    In the pursuit of blood tests that can detect mutations responsible for FTD, Dr. Rosa Rademakers has found a disconnect between levels of blood markers for Chromosome 9 mutation orf72 and levels in brain tissue markers. This means that testing for this mutation’s severity won’t be possible through a relatively easy-to-obtain blood sample. Such may not be the case for other genetic mutations associated with FTD, but it is an important new point to guide the search for early detection methods.

    Dr. Rademakers’ lab has done all sorts of work to elucidate how that C9orf72 gene can lead to the brain deterioration, and one important new clue is that homeobox genes, which work neuronal repair and regeneration, seem to respond to the C9orf72 abnormality. Do those homeobox (“HOX” if you want to google or pubmed search it) genes need a boost in order for patients to compensate for their dementia? These results are so fresh that they are being presented in posters at the conference, which often precedes their publication in a medical journal for 6-12 months.

    International collaboration to consolidate progranulin mutation carriers (different chromosome and gene from C9orf72) has brought 555 mutation carriers DNA together for analysis – more to come in the future. The largest families with FTD have yielded the previously described progranulin, C9orf72, fused in sarcoma (FUS), MAPT (tau), CHMP2B, or valosin-containing protein (VCP) mutations. This is roughly 20% of known FTD cases followed in Antwerp.
    The Mayo Clinic (Dr. Rademakers’ home base) has 170 brains from patients with TDP-43 proteinopathy (frequently a result of progranulin mutation), and whole-genome sequencing is under way. This has identified 2 new mutations related to the ALS-variant of FTD, a mutation on chromosome *10* in a gene that codes for protein optineurin (OPTN). A candidate gene under examination but NOT YET PROVEN to have a strong or likely causal association to FTD is KIF-17.

    Dr. Christine van Broeckhoven from the Univ of Antwerp reported from her lab:

  • in their search for which genetic factors determine the earlier ages at onset of FTD, they have not seen a role for serum levels of progranulin protein. Instead, it seems that one particular part of the genome may be responsible for assigning a person’s onset age. The next steps are to correlate this with something more easily identifiable in either serum or cerebrospinal fluid (obtained through lumbar puncture).
  • Among cases with C9orf72 mutations, they report that short repeat sequences seem to be more associated with anticipation between generations, which is the phenomenon of a child having earlier onset age than an affected parent. This is significant as the opposite of what happens in a disease like Huntington’s, in which more repeats means earlier onset of illness. If you’re a genetics junkie, you may be interested to know that the degree of repeats affects the methylation status of the DNA processing.
  • another candidate gene, FLNC, makes protein filamin C. The expression of this gene is increased in TDP-43 patients, so it may be a secondary villain in taking down the integrity of cell structure and ability to communicate.
  • another candidate gene: VPS13C may work independent of the aforementioned genetic mutations. It’s been identified in a few families and some patients without family history. Dr. Stephanie Philtjens reported further on the clinical presentations of patients with this mutation. Onset ages were 62 years on average, with two cases manifesting in their early 40s. About half of patients were women, no gender bias. There is decreased VPS13C protein in patients with the mutation, but what the protein is normally doing in relation to preventing dementia remains unclear. There may be a link to Alzheimer’s disease as well. Genetics junkies may recall that CHMP2B is another gene for VPS, which has an established link to FTD.
  • work continues to understand how mutations in SQSTM1 lead to ALS or other neurodegenerative disorders. This one doesn’t have a single association to illness; variants in the mutation lead patients to different fates.

    Carrying on from the SQSTM1 theme above, Dr. Paul Taylor described ongoing work on the association between inclusion body myopathy (IBM), Paget’s disease of bone, and familial cases of ALS. Matrin 3 mutations can be responsible for this presentation, but Dr. Taylor has been working most on VCP. The protein will ordinarily act as the remodeler of multimeric complexes. That’s a mouthful that I can really only translate for you as helping to keep working surfaces within the cell functioning to traffic proteins appropriately. In the presence of the mutation, cells pocket TDP-43. For genetics junkies, VCP in this context is gumming up hnRNPA species 1 and 2B1.
    The exciting part of this work is the similarity of glycine-rich segments of the hnRNPAs to yeast prions. You may have heard of prions before, in the context of mad cow disease or Creutzfeld-Jakob disease. Neil Cashman out here at UBC has been arguing in favor of a prion mechanism turning dementias (not just FTD) on at a certain point in life, based on genetic vulnerabiltiies and environmental exposures. Dr. Taylor explained that the prion-like portions of the hnRNPAs may be the place where that switching-on may transpire, resulting immediately (at least in his videos) of key proteins precipitating out of solution into granules loaded with proteinopathy! The good news is that the switch can go in the other direction, OFF, so his lab is hot on the trail of how to control that switch. In a Petri dish, they can use a laser to disassemble the granules, but the presence of VCP locks the switch to ON.

  • Follow-Up Report for Non-Fluent PPA Intervention

    I’ve posted before about the promising work of Dr. Roy Hamilton at Penn. In Spring, he described an ongoing trial of tDCS (a form of non-invasive brain stimulation) to suppress a small area of the brain’s right hemisphere to enhance speech. At that time, he had positive effects on fluency when an instrument called the Western Aphasia Battery was used before and after the treatments. A paper on this same intervention used in the context of aphasia resulting from stroke has already been published. I hope there will be a further update for PNFA at the international FTD conference, which starts tomorrow in Vancouver.

    Having a Conversation with a Patient

    There are many times that friends or family members would like to visit the patient but don’t quite know how to start a conversation that will be meaningful or adapted to the patient’s communication ability. There’s help available: Very specific how-to info in Claudia Strauss’ Talking to Alzheimer’s: Simple Ways to Connect When You Visit with a Family Member or Friend. It’s actually been around since 2001, but the advice holds true.