What Does Alzheimer’s Do To the Human Brain?

What Does Alzheimer’s Do To the Human Brain?


Alzheimer’s disease is the most common cause
of dementia in the world. Nearly 50 million people worldwide
have it, and every 66 seconds someone in the United States
is diagnosed with it. It’s been called the epidemic of our century,
but even after decades of research, finding a way to
prevent this disease has been a puzzle that has eluded the medical community. Now, we may
be closer than ever to solving it. – I personally have a lot of hope that we
will see the first survivors of Alzheimer’s disease in our
lifetime. I’m Nilüfer Ertekin-Taner. I’m a neurologist and I’m a neuroscientist
focused on Alzheimer’s disease and related dementias. Alzheimer’s disease is a progressive condition,
typically starting in the part of the brain associated with memory. It then spreads, causing trouble with memory,
cognitive abilities and eventually, loss of bodily functions. It’s a relentlessly progressive condition
that leads to death by or with the disease. Age is the most common risk factor for Alzheimer’s. In fact, about a third of individuals ages
85 or above have it. And while the exact onset of this disease
is not known, what is known is that it is characterized by a buildup of toxic proteins
in the brain. – There are two main hallmarks of Alzheimer’s
disease in the brain. One of them is amyloid
beta, which builds up in plaques outside of neurons. And the other one is tau, which is a fibrillar
protein, which builds up inside of neurons. Both of these proteins are toxic, and ultimately
they lead to dysfunction and death of neurons. As these proteins accumulate and neurons start
to die, the brain’s immune system kicks into gear. – The immune cells of the brain, called microglia,
try to get rid of these toxic protein substances. And they also try to get rid of the dead neurons. Ultimately, this immune response leads to
chronic inflammation of the brain. Over a longer
period of time, as the disease progresses and neural cell death continues, the affected
brain regions begin to shrink. And that’s about when symptoms start to
show. – Although it starts typically in areas that
affect our memory, ultimately it starts affecting areas
that control our movements, that control our swallowing and our breathing. And in the terminal
stages of this condition, our patients with Alzheimer’s disease lose their ability to
move, and they become bedbound. And at the end our patients unfortunately
succumb to pneumonia, malnutrition, generalized sepsis of the body. And this is all because of Alzheimer’s disease
and what it does in the brain. And while this all sounds dire, decades of
studies on patients show that there may be a window
of opportunity to prevent the condition advancing before you would see any symptoms. – We know that 10 or 20 years before the symptoms
of Alzheimer’s disease can be observed, there are changes in the brain. We know this from biomarker studies looking
at levels of abnormal proteins in the spinal fluid, in the brain,
or in blood. So biomarkers are quantifiable measures that
can help us detect disease or an aspect of the disease. So for example, we can think blood glucose
levels as being a biomarker for diabetes. We can think about blood pressure measurements
as being a biomarker for high blood pressure. In the same vein, we have developed, and continue
to develop biomarkers for Alzheimer’s disease. And while these biomarkers are important to
follow the disease’s progression the research is still ongoing. Right now, knowing a patient’s risk factors
can help them make choices to slow the onset of Alzheimer’s. – Those risk factors that are bad for your
heart are generally bad for your brain. So diabetes,
hypertension, smoking and obesity are risk factors for Alzheimer’s disease. On the flip side,
What we recommend to our patients, and even the general public is that they stay engaged,
both cognitively, physically and socially. That can be anything from exercise to maintaining
a strong social network. The takeaway
seems to be: stay active. – We are also at an amazing time in research
and clinical studies. We are able to combine clinical
information with very complex genetic and other molecular information. This helps us try and
identify the very complex molecular perturbations that can lead to this condition.

Author: Kevin Mason

15 thoughts on “What Does Alzheimer’s Do To the Human Brain?

  1. https://www.ncbi.nlm.nih.gov/pubmed/28217094

    Front Pharmacol. 2017 Feb 3;8:20. doi: 10.3389/fphar.2017.00020. ECollection 2017

    In Vivo Evidence for Therapeutic Properties of Cannabidiol (CBD) for Alzheimer's Disease. Watt G1, Karl T2

    Alzheimer's disease (AD) is a debilitating neurodegenerative disease that is affecting an increasing number of people. It is characterized by the accumulation of amyloid-β and tau hyperphosphorylation as well as neuroinflammation and oxidative stress. Current AD treatments do not stop or reverse the disease progression, highlighting the need for new, more effective therapeutics. Cannabidiol (CBD) is a non-psychoactive phytocannabinoid that has demonstrated neuroprotective, anti-inflammatory and antioxidant properties in vitro. Thus, it is investigated as a potential multifunctional treatment option for AD. Here, we summarize the current status quo of in vivo effects of CBD in established pharmacological and transgenic animal models for AD.

    The studies demonstrate the ability of CBD to reduce reactive gliosis and the neuroinflammatory response as well as to promote neurogenesis. Importantly, CBD also reverses and prevents the development of cognitive deficits in AD rodent models. Interestingly, combination therapies of CBD and Δ9-tetrahydrocannabinol (THC), the main active ingredient of cannabis sativa, show that CBD can antagonize the psychoactive effects associated with THC and possibly mediate greater therapeutic benefits than either phytocannabinoid alone. The studies provide "proof of principle" that CBD and possibly CBD-THC combinations are valid candidates for novel AD therapies. Further investigations should address the long-term potential of CBD and evaluate mechanisms involved in the therapeutic effects described.

    https://youtu.be/sb6g5-A1ljA  Alzheimer’s b4 and after CBD

    https://youtu.be/yOPLmcFsQ0k  Before and after mental illness Alzheimer’s

    https://youtu.be/KEkvOrtC4lo  CBD oil, Dad’s first dose

    https://youtu.be/q5zX947d9dE  CBD provides help for Alzheimer’s sufferers 

    https://youtu.be/lD74d-S2dH0  Treating dementia and Alzheimer’s – Interview on the effects of CBD on Alzheimer’s and mental illness 

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4326479/ 

    Nutrition Journal
    BioMed Central
    Role of homocysteine in the development of cardiovascular disease
    Paul Ganguly and Sreyoshi Fatima Alam

    B)
    The direct effect of homocysteine on the nervous system:
    The action of homocysteine as a neurotransmitter: homocysteine and its related compounds may have a role as an excitatory agonist on the NMDA subtype of glutamate receptors and recent evidence also points to the involvement of NMDA modulatory sites [11]. It has also been shown that homocysteine, besides acting as a partial agonist at glutamate receptors also acts as a partial antagonist of glycine co-agonist site of the NMDA receptor [11]. In the presence of normal glycine levels and normal physiological conditions homocysteine does not cause toxicity below millimolar concentrations. However in case of a head trauma or stroke, there is an elevation in glycine levels in which instance the neurotoxic effect of homocysteine as an agonist outweighs its neuroprotective antagonist effect. This may cause neuronal damage via calcium ion influx or free radical generation [11].

    One evaluative experiment to discover the direct effect of homocysteine on the central nervous system involved local application of homocysteine by two different methods of drug delivery to the central nervous system of rats- pressure ejection and ionophoresis [12]. Extracellular recordings were taken from neurons of cerebral cortex, cerebellum and midbrain. The recordings after either method of administration portrayed a dose-dependent increase in neuronal activity by D, L-homocysteine and L-glutamate in 67% of cells tested with both drugs. The similarity in the dose required of D,L-homocysteine and L-Glutamate, points out that D,L-homocysteine seems to be as potent as the latter. This data indicates that homocysteine seems to have an excitatory action on neurons, and this finding may account for neurological symptoms associated with disorders of amino acid metabolism [12]. Some studies also suggest that elevated homocysteine levels may be associated with alterations in mental health such as cognitive impairment, dementia, depression, Alzheimer’s and Parkinson’s disease [2, 11].

  2. Hmmm there are a couple downvotes. That must be the science is completely wrong. I guess I can't rely on this video

  3. Isn't known that marijuana reduces plaque and inflammation in the brain? British medical journal and California research…

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