[jcitron]

Hi all,

I have some questions regarding dementia and this has to do with my dad. He's 72 going on 73 and has been acting weird lately. These symptoms come and go and over time they have gotten worse. My mom is at wits' end because she gets the brunt of the results.

---- He forgets names, dates, and places often.

---- Forgets where he places things.
We've ended up purchasing more than two of many things because he miss-placed them. We never let him put things away anymore if we can help it.

---- He makes up stories and greatly exaggerates the truth of old incidents

---- Gets past incidents mixed up to a point where they're totally misconstrued. See above

---- Gets very beligerent and really argumentative
Looks for things to argue over or fight about. They're stupid things like changing channels on the TV.

---- Sleeps a lot.
Gets up feeds the cats, complains about all the hard work he has to do and takes a nap.


---- Constant eating.
He eats more in one day than I consume in a week.
It's mostly carbs and other sweets, which kind of scares me. Diabetes?

---- Talks to himself constantly.
Not like the occasional "You idiot, remember the car keys", or "Oh yeah, you need to water the plants, etc." This is full conversations with the man in the mirror or while feeding the cats.

---- Eating out of children's plates. The kind with the divisors that we bought for me neice and nephews.
Why?

---- Very obsessive compulsive over certain routines.
If someone gets in the bathroom before he cleans the catbox, he goes ballistic. If the pets or wildlife need food and there isn't any in the closet, he goes bonkers until we bring him out to buy some. (It's not like the cats need to eat; they're well fed and content, and the deer and turkeys can wait a day or two).

---- Always off in his own world.
He acts like he's off on his own planet all the time.

From a side point, he does have some mild hypertension and is taking medication for that. He also complains all the time about aches and pains, but because he complains so much, we don't know if this is real.

I keep thinking about his carbs and sugar intake. Could this be diabetes, or some other sugar-related imbalance?

So anyway, we're going crazy. My mom is ready to walk away from 49 years of marriage. She's been on the receiving end of this for quite a long time. We don't know what's wrong, or how to handle this. How would I go about getting him to a doctor, etc? I'm overwhelmed with this as well and don't need the extra stress.

Thanks in advance as always,

John

[reverett123]

I might add that curcumin/turmeric has a similar action

http://www.sciencedaily.com/releases...0109091102.htm

Reversal Of Alzheimer's Symptoms Within Minutes In Human Study

PET Scan of Alzheimer's Disease Brain. (Credit: NIH/National Institute On Aging)

ScienceDaily (Jan. 9, 2008) — An extraordinary new scientific study, which for the first time documents marked improvement in Alzheimer’s disease within minutes of administration of a therapeutic molecule, has just been published in the Journal of Neuroinflammation.

This new study highlights the importance of certain soluble proteins, called cytokines, in Alzheimer’s disease. The study focuses on one of these cytokines, tumor necrosis factor-alpha(TNF), a critical component of the brain’s immune system. Normally, TNF finely regulates the transmission of neural impulses in the brain. The authors hypothesized that elevated levels of TNF in Alzheimer’s disease interfere with this regulation. To reduce elevated TNF, the authors gave patients an injection of an anti-TNF therapeutic called etanercept. Excess TNF-alpha has been documented in the cerebrospinal fluid of patients with Alzheimer’s.

The new study documents a dramatic and unprecedented therapeutic effect in an Alzheimer’s patient: improvement within minutes following delivery of perispinal etanercept, which is etanercept given by injection in the spine. Etanercept (trade name Enbrel) binds and inactivates excess TNF. Etanercept is FDA approved to treat a number of immune-mediated disorders and is used off label in the study.

The use of anti-TNF therapeutics as a new treatment choice for many diseases, such as rheumatoid arthritis and potentially even Alzheimer’s, was recently chosen as one of the top 10 health stories of 2007 by the Harvard Health Letter.

Similarly, the Neurotechnology Industry Organization has recently selected new treatment targets revealed by neuroimmunology (such as excess TNF) as one of the top 10 Neuroscience Trends of 2007. And the Dana Alliance for Brain Initiatives has chosen the pilot study using perispinal etanercept for Alzheimer’s for inclusion and discussion in their 2007 Progress Report on Brain Research.

The lead author of the study, Edward Tobinick M.D., is an assistant clinical professor of medicine at the University of California, Los Angeles and director of the Institute for Neurological Research, a private medical group in Los Angeles. Hyman Gross, M.D., clinical professor of neurology at the University of Southern California, was co-author.

The study is accompanied by an extensive commentary by Sue Griffin, Ph.D., director of research at the Donald W. Reynolds Institute on Aging at the University of Arkansas for Medical Sciences (UAMS) in Little Rock and at the Geriatric Research and Clinical Center at the VA Hospital in Little Rock, who along with Robert Mrak, M.D., chairman of pathology at University of Toledo Medical School, are editors-in-chief of the Journal of Neuroinflammation.

Griffin and Mrak are pioneers in the field of neuroinflammation. Griffin published a landmark study in 1989 describing the association of cytokine overexpression in the brain and Alzheimer’s disease. Her research helped pave the way for the findings of the present study. Griffin has recently been selected for membership in the Dana Alliance for Brain Initiatives, a nonprofit organization of more than 200 leading neuroscientists, including ten Nobel laureates.

“It is unprecedented that we can see cognitive and behavioral improvement in a patient with established dementia within minutes of therapeutic intervention,” said Griffin. “It is imperative that the medical and scientific communities immediately undertake to further investigate and characterize the physiologic mechanisms involved. This gives all of us in Alzheimer’s research a tremendous new clue about new avenues of research, which is so exciting and so needed in the field of Alzheimer’s. Even though this report predominantly discusses a single patient, it is of significant scientific interest because of the potential insight it may give into the processes involved in the brain dysfunction of Alzheimer’s.”

While the article discusses one patient, many other patients with mild to severe Alzheimer’s received the treatment and all have shown sustained and marked improvement.

The new study, entitled “Rapid cognitive improvement in Alzheimer’s disease following perispinal etanercept administration,” and the accompanying commentary, entitled “Perispinal etanercept: Potential as an Alzheimer’s therapeutic,” are available on the Web site of the Journal of Neuroinflammation (http://www.jneuroinflammation.com/co...5/1/2/abstract).

[reverett123]

The link at the end of the above lets you download the full text and it is very interesting. I had assumed that this was an anti-inflammatory action, but numbers 4 and 5 below open up some new ideas that might apply directly to PD as well.


The authors' preferred hypothesis to explain the rapid
clinical improvement observed centers on the emerging
evidence, which suggests that TNF-alpha is of critical
importance in the regulation of synaptic transmission in
the brain. The authors are led in this direction by the com-
bination of:
1. The extreme rapidity of the effect;
2. The extraordinary potency and selectivity of etanercept
as an anti-TNF-alpha agent, due to its biologic nature and
molecular structure;
3. The various lines of scientific evidence which have sug-
gested that synaptic dysfunction may be of key impor-
tance in the pathogenesis of Alzheimer's disease [28-32];
4. Evidence suggesting that TNF-alpha regulates synaptic
transmission in the brain[33-35,42,43]; and,
5. Evidence suggesting that TNF-alpha mediates the syn-
aptic dysfunction underlying cognitive and behavioral
impairment produced by both beta-amyloid and beta-
amyloid oligomers [36,37].

[reverett123]

1: Pharmazie. 2007 Dec;62(12):937-42.

Neuroprotective effect of curcumin is mainly mediated by blockade of microglial
cell activation.

Lee HS, Jung KK, Cho JY, Rhee MH, Hong S, Kwon M, Kim SH, Kang SY.

Pharmacology Department, National Institute of Toxicological Research, KFDA,
Seoul, South Korea.

Curcumin, the major yellow pigment in turmeric (Curcuma longa), is a
well-documented naturally-occurring anti-oxidant with numerous pharmacological
activities such as anti-inflammatory, anti-carcinogenic and anti-bacterial
effects. In this study, curcumin's neuroprotective effect was carefully examined
using a coculture system, based on reports that curcumin-containing plants are
neuroprotective. Coculturing neuronal cells and activated microglial cells
enhanced dopamine-induced neuronal cell death from 30% up to 50%. However,
curcumin did not protect dopamine-directed neuronal cell death and sodium
nitroprosside (SNP)-induced NO generation, but only blocked activated microglial
cell-mediated neuronal cell damage under inflammatory conditions. Indeed,
curcumin blocked the production of pro-inflammatory and cytotoxic mediators such
as NO, TNF-alpha, IL-1alpha, and IL-6 produced from Abeta(25-35)/IFN-gamma- and
LPS-stimulated microglia, in a dose-dependent manner. Therefore, our results
suggest that curcumin-mediated neuroprotective effects may be mostly due to its
anti-inflammatory effects.


PMID: 18214347 [PubMed - indexed for MEDLINE]

[reverett123]

1: Neuroreport. 2007 Oct 29;18(16):1725-8.

Dopamine induces TNFalpha and TNF-R1 expression in SH-SY5Y human neuroblastoma
cells.

Gómez-Santos C, Francisco R, Giménez-Xavier P, Ambrosio S.

Biochemistry Unit, Department of Physiological Sciences II, University of
Barcelona - IDIBELL, Barcelona, Spain.

Cytotoxic concentrations of dopamine (100-500 microM DA) induce expression of
tumour necrosis factor receptor-1 (TNF-R1) and tumour necrosis factor-alpha
(TNFalpha) in SH-SY5Y human neuroblastoma cells. TNFalpha expression is
dose-dependent and can also be detected after 6-hydroxydopamine (6-OHDA) or
1-methyl-4-phenylpyridinium iodide (MPP) treatment. The expression of TNF-R1 is
also dose-dependent, but was not observed in 6-OHDA or MPP-treatment. Cells not
expressing TNF-R1 were insensitive to TNFalpha, whereas those treated with DA
showed a further decrease in viability when subsequently treated with TNFalpha.
Thus, DA treatment confers sensitivity to TNFalpha. The decrease of cell
viability caused by DA was in part prevented by neutralizing TNFalpha with
anti-TNFalpha. As TNF-R1 is increased in substantia nigra of Parkinsonian brains,
we suggest that nonvesiculated DA might also play a role in inducing TNF-R1
expression and predispose the neuron to the action of cytokines released in a
microglia-mediated inflammatory response.


PMID: 17921876 [PubMed - indexed for MEDLINE]

[reverett123]

I just realized that I hijacked this thread. Got swept up in the excitement! In for a dime - in for a dollar, though:

Green tea compounds also block TNF.

The most important thing to me is the part about TNF interfering with transmission of signal at the synapses. Also, the fact that the anti-TNF compounds are dose dependent. Just because we took one tablet and nothing happened doesn't mean that there was nothing there.

[jcitron]

Thanks Rick for the information. I'll pass this on to my mom maybe she can cook up something with tumeric in it.

I did find the link to Science Daily interesting though. I may bookmark that site for future reading.

John

[jcitron]

~Bump~

Does anyone else have any thoughts?

Thanks!

John

[gaykir]

John - just bumping this up because I think Rick's response was long enough that most folks probably zoned out

Sounds like classic alzheimer's to me (unless he's a Parkie on too much agonist...)

[Curious]

Originally Posted by jcitron

~Bump~

Does anyone else have any thoughts?

Thanks!

John

john...has he had his testosterone levels checked? low test can cause signs of depression...and your dad has those signs.

i'll find the link to the article.

thanks for the bump.