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Aubrey D.N.J. de Grey, Ph.D.
Chief Science Officer
SENS Research Foundation
aubrey@sens.org
http://www.sens.org/
Most infectious diseases have been easily
prevented
 Sanitation
 Vaccines
 Antibiotics
 Carrier control
Age-related diseases have not. Why not?
reduced light adaptation
reduced ethanol metabolism
altered drug pharmacokinetics
somatopause
loss of cardiac adaptability
incontinence
impaired wound healing
idiopathic axonal polyneuropathy
autonomic neuropathy
arrhythmia
chronic obstructive pulmonary disorder
benign prostatic hypertrophy
menopause
leukoaraiosis
stroke
vascular dementia
frontotemporal dementia
immunosenescence
anosmia
cachexia
anorexia of aging
systolic hypertension
ageusia
erectile dysfunction
orthostatic hypotension
impaired adaptive beta-cell proliferation
fibroblast collapse
anergic T-cell clones
cellular senescence
vascular calcification
impaired transdermal absorption
impaired thermoregulation
reduced tactile acuity
impaired vasoconstriction
loss of neuromuscular junctions
delayed withdrawal reflex
impaired pH maintenance
reduced chemical clearance
altered dermal immune cell residence and function
aberrant allergic and irritant reactions
loss of skin elasticity
impaired vitamin D synthesis
reduced renal reserve
renal cortex atrophy
gut dysbiosis
loss of jejunal villus height
impaired response to vaccination
impaired thirst
lentigo senilis
thinning hair
impaired proprioception
impaired balance
reduced vital capacity
reduced cardiorespiratory endurance
impaired sweat response
impaired blood distribution
nutrient malabsorption
diverticular disease
presbyphagia
increased reflux
alveolar loss
neuronal loss
senile emphysema
degenerative disc disease
joint calcification
pineal calcification
aberrant differentiation
gait instability
frontal demyelination
axonal atrophy
impaired functional connectivity
impaired working memory
presbycusis
osteoporosis
osteoarthritis
autoimmunity
greying hair
presbyopia
cataract
glaucoma
temporal arteritis
polymyalgia rheumatica
wrinkling
Alzheimer's disease
Pick's disease
corticobasal degeneration
progressive supranuclear palsy
Parkinson's disease
multiple system atrophy
dementia with Lewy bodies
sarcopenia
glomerulonephritis
senile cardiac amyloidosis
atherosclerosis
arteriosclerosis
age-related macular degeneration
cardiomyopathy
diastolic heart failure
cancer
systemic inflammation
oxidative stress
reduced coronary blood flow
loss of cardiac reserve
andropause
thymic involution
reduced plasma renin activity
reduced aldosterone
reduced melatonin diurnal rhythm
Aging is:
The life-long accumulation of “damage” to
the body that occurs as an intrinsic side-
effect of the body’s normal operation.
The body can tolerate some damage, but
too much of it causes disease and disability.
PathologyMetabolism Damage
(life-long) (late life)
Diseases Aging
Communicable Congenital Chronic
Tuberculosis
Malaria
HIV
…
Tay-Sachs
MELAS
Li-Fraumeni
...
Alzheimer’s
Cancer
Atherosclerosis
…
Frailty
Sarcopenia
Immunosenescence
…
Diseases Aging
Communicable Congenital Specific General
Tuberculosis
Malaria
HIV
…
Tay-Sachs
MELAS
Li-Fraumeni
...
Alzheimer’s
Cancer
Atherosclerosis
…
Frailty
Sarcopenia
Immunosenescence
…
Pathology
Geriatrics
Metabolism Damage
(life-long) (late life)
Pathology
Gerontology Geriatrics
Metabolism Damage
(life-long) (late life)
Pathology
Gerontology Geriatrics
Metabolism Damage
Maintenance
(life-long) (late life)
Cell loss, cell atrophy
Division-obsessed cells
Death-resistant cells
Mitochondrial mutations
Intracellular junk
Extracellular junk
Extracellular matrix stiffening
No new type of
damage
confirmed
since 1982
And, I’ve said
so without
challenge
since 2002
Damage type
Why? That was easy
How? That’s where we have a new plan
What? That’s where we show you it’s a
good plan (can be done, is being done)
Cell loss, cell atrophy
Division-obsessed cells
Death-resistant cells
Mitochondrial mutations
Intracellular junk
Extracellular junk
Extracellular matrix stiffening
Cell therapy, mainly
Telomerase/ALT gene deletion
plus periodic stem cell reseeding
Suicide genes, immune stimulation
Allotopic expression of 13 proteins
Transgenic microbial hydrolases
Phagocytosis by immune stimulation
AGE-breaking molecules/enzymes
Damage type The maintenance approach
 Total synthesis of glucosepane, allowing identification
of antibodies and degraders (Science, 2015)
 Modified bacterial enzyme protects cells from
atherogenic oxysterols (Biotech Bioeng, 2012)
 Catalytic antibodies cleave cardiotoxic amyloid (J Biol
Chem, 2014)
 Much more ongoing in our research centre and
funded labs
See their names, their awesome
credentials and their hard-hitting
endorsement of our research
approach at
www.sens.org/about/leadership/resea
Cell loss, cell atrophy
Division-obsessed cells
Death-resistant cells
Mitochondrial mutations
Intracellular junk
Extracellular junk
Extracellular matrix stiffening
Cell therapy, mainly
Telomerase/ALT gene deletion
plus periodic stem cell reseeding
Suicide genes, immune stimulation
Allotopic expression of 13 proteins
Transgenic microbial hydrolases
Phagocytosis by immune stimulation
AGE-breaking molecules/enzymes
Damage type The maintenance approach
Endothelial cell
Lipid-
engorged
lysosome
Foam
cell
Mathieu et al., Biotechnol. Bioeng. 2012; 109(9):2409-2415
Available at Amazon and all good book stores.
Paperback is cheaper, and has an extra chapter!
Visit us on the web at
http://www.sens.org/
Read the (semi-technical) book.
Drop us a line at
foundation@sens.org
Learn more
www.sens.org
aubrey@sens.org

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Aubrey de Grey's Slide - Nigeria ICT Fest 2015

  • 1. Aubrey D.N.J. de Grey, Ph.D. Chief Science Officer SENS Research Foundation aubrey@sens.org http://www.sens.org/
  • 2. Most infectious diseases have been easily prevented  Sanitation  Vaccines  Antibiotics  Carrier control Age-related diseases have not. Why not?
  • 3. reduced light adaptation reduced ethanol metabolism altered drug pharmacokinetics somatopause loss of cardiac adaptability incontinence impaired wound healing idiopathic axonal polyneuropathy autonomic neuropathy arrhythmia chronic obstructive pulmonary disorder benign prostatic hypertrophy menopause leukoaraiosis stroke vascular dementia frontotemporal dementia immunosenescence anosmia cachexia anorexia of aging systolic hypertension ageusia erectile dysfunction orthostatic hypotension impaired adaptive beta-cell proliferation fibroblast collapse anergic T-cell clones cellular senescence vascular calcification impaired transdermal absorption impaired thermoregulation reduced tactile acuity impaired vasoconstriction loss of neuromuscular junctions delayed withdrawal reflex impaired pH maintenance reduced chemical clearance altered dermal immune cell residence and function aberrant allergic and irritant reactions loss of skin elasticity impaired vitamin D synthesis reduced renal reserve renal cortex atrophy gut dysbiosis loss of jejunal villus height impaired response to vaccination impaired thirst lentigo senilis thinning hair impaired proprioception impaired balance reduced vital capacity reduced cardiorespiratory endurance impaired sweat response impaired blood distribution nutrient malabsorption diverticular disease presbyphagia increased reflux alveolar loss neuronal loss senile emphysema degenerative disc disease joint calcification pineal calcification aberrant differentiation gait instability frontal demyelination axonal atrophy impaired functional connectivity impaired working memory presbycusis osteoporosis osteoarthritis autoimmunity greying hair presbyopia cataract glaucoma temporal arteritis polymyalgia rheumatica wrinkling Alzheimer's disease Pick's disease corticobasal degeneration progressive supranuclear palsy Parkinson's disease multiple system atrophy dementia with Lewy bodies sarcopenia glomerulonephritis senile cardiac amyloidosis atherosclerosis arteriosclerosis age-related macular degeneration cardiomyopathy diastolic heart failure cancer systemic inflammation oxidative stress reduced coronary blood flow loss of cardiac reserve andropause thymic involution reduced plasma renin activity reduced aldosterone reduced melatonin diurnal rhythm
  • 4. Aging is: The life-long accumulation of “damage” to the body that occurs as an intrinsic side- effect of the body’s normal operation. The body can tolerate some damage, but too much of it causes disease and disability.
  • 6. Diseases Aging Communicable Congenital Chronic Tuberculosis Malaria HIV … Tay-Sachs MELAS Li-Fraumeni ... Alzheimer’s Cancer Atherosclerosis … Frailty Sarcopenia Immunosenescence …
  • 7. Diseases Aging Communicable Congenital Specific General Tuberculosis Malaria HIV … Tay-Sachs MELAS Li-Fraumeni ... Alzheimer’s Cancer Atherosclerosis … Frailty Sarcopenia Immunosenescence …
  • 10.
  • 12. Cell loss, cell atrophy Division-obsessed cells Death-resistant cells Mitochondrial mutations Intracellular junk Extracellular junk Extracellular matrix stiffening No new type of damage confirmed since 1982 And, I’ve said so without challenge since 2002 Damage type
  • 13. Why? That was easy How? That’s where we have a new plan What? That’s where we show you it’s a good plan (can be done, is being done)
  • 14. Cell loss, cell atrophy Division-obsessed cells Death-resistant cells Mitochondrial mutations Intracellular junk Extracellular junk Extracellular matrix stiffening Cell therapy, mainly Telomerase/ALT gene deletion plus periodic stem cell reseeding Suicide genes, immune stimulation Allotopic expression of 13 proteins Transgenic microbial hydrolases Phagocytosis by immune stimulation AGE-breaking molecules/enzymes Damage type The maintenance approach
  • 15.  Total synthesis of glucosepane, allowing identification of antibodies and degraders (Science, 2015)  Modified bacterial enzyme protects cells from atherogenic oxysterols (Biotech Bioeng, 2012)  Catalytic antibodies cleave cardiotoxic amyloid (J Biol Chem, 2014)  Much more ongoing in our research centre and funded labs
  • 16. See their names, their awesome credentials and their hard-hitting endorsement of our research approach at www.sens.org/about/leadership/resea
  • 17.
  • 18.
  • 19. Cell loss, cell atrophy Division-obsessed cells Death-resistant cells Mitochondrial mutations Intracellular junk Extracellular junk Extracellular matrix stiffening Cell therapy, mainly Telomerase/ALT gene deletion plus periodic stem cell reseeding Suicide genes, immune stimulation Allotopic expression of 13 proteins Transgenic microbial hydrolases Phagocytosis by immune stimulation AGE-breaking molecules/enzymes Damage type The maintenance approach
  • 21. Mathieu et al., Biotechnol. Bioeng. 2012; 109(9):2409-2415
  • 22. Available at Amazon and all good book stores. Paperback is cheaper, and has an extra chapter! Visit us on the web at http://www.sens.org/ Read the (semi-technical) book. Drop us a line at foundation@sens.org Learn more